Subjects -> MEDICAL SCIENCES (Total: 8529 journals)
    - ANAESTHESIOLOGY (120 journals)
    - CARDIOVASCULAR DISEASES (332 journals)
    - DENTISTRY (292 journals)
    - ENDOCRINOLOGY (150 journals)
    - FORENSIC SCIENCES (41 journals)
    - HEMATOLOGY (155 journals)
    - HYPNOSIS (4 journals)
    - INTERNAL MEDICINE (167 journals)
    - MEDICAL GENETICS (58 journals)
    - MEDICAL SCIENCES (2342 journals)
    - NURSES AND NURSING (362 journals)
    - OBSTETRICS AND GYNECOLOGY (207 journals)
    - ONCOLOGY (381 journals)
    - OTORHINOLARYNGOLOGY (82 journals)
    - PATHOLOGY (98 journals)
    - PEDIATRICS (273 journals)
    - PSYCHIATRY AND NEUROLOGY (822 journals)
    - RESPIRATORY DISEASES (103 journals)
    - RHEUMATOLOGY (78 journals)
    - SPORTS MEDICINE (81 journals)
    - SURGERY (401 journals)

RESPIRATORY DISEASES (103 journals)                     

Showing 1 - 104 of 104 Journals sorted alphabetically
Advances in Respiratory Medicine     Open Access   (Followers: 7)
Advances in Thoracic Diseases     Open Access  
American Journal of Respiratory and Critical Care Medicine     Full-text available via subscription   (Followers: 257)
American Journal of Respiratory Cell and Molecular Biology     Full-text available via subscription   (Followers: 20)
American Review of Respiratory Disease     Full-text available via subscription   (Followers: 4)
Angiologia e Cirurgia Vascular     Open Access   (Followers: 1)
Annals of the American Thoracic Society     Full-text available via subscription   (Followers: 17)
Annals of Thoracic Medicine     Open Access   (Followers: 6)
Archives of Pulmonology and Respiratory Care     Open Access   (Followers: 1)
Archivos de Bronconeumología     Full-text available via subscription  
Archivos de Bronconeumología (English Edition)     Full-text available via subscription   (Followers: 1)
Asthma Research and Practice     Open Access   (Followers: 2)
BMC Pulmonary Medicine     Open Access   (Followers: 5)
BMJ Open Respiratory Research     Open Access   (Followers: 7)
Breathe     Open Access   (Followers: 5)
Canadian Journal of Respiratory, Critical Care, and Sleep Medicine     Hybrid Journal   (Followers: 1)
Canadian Respiratory Journal     Open Access   (Followers: 3)
Case Reports in Pulmonology     Open Access   (Followers: 3)
Chest     Full-text available via subscription   (Followers: 102)
Chest Disease Reports     Open Access   (Followers: 2)
Chronic Respiratory Disease     Hybrid Journal   (Followers: 9)
Clinical Lung Cancer     Hybrid Journal   (Followers: 6)
Clinical Medicine Insights : Circulatory, Respiratory and Pulmonary Medicine     Open Access   (Followers: 3)
Clinical Pulmonary Medicine     Hybrid Journal   (Followers: 2)
COPD Research and Practice     Open Access   (Followers: 1)
COPD: Journal of Chronic Obstructive Pulmonary Disease     Hybrid Journal   (Followers: 16)
Current Opinion in Pulmonary Medicine     Hybrid Journal   (Followers: 10)
Current Pulmonology Reports     Hybrid Journal  
Current Research in Tuberculosis     Open Access   (Followers: 3)
Current Respiratory Care Reports     Hybrid Journal   (Followers: 2)
Current Respiratory Medicine Reviews     Hybrid Journal   (Followers: 5)
Der Pneumologe     Hybrid Journal   (Followers: 1)
Egyptian Journal of Chest Diseases and Tuberculosis     Open Access   (Followers: 3)
ERJ Open Research     Open Access   (Followers: 3)
Eurasian Journal of Pulmonology     Open Access  
European Clinical Respiratory Journal     Open Access   (Followers: 4)
European Respiratory Journal     Full-text available via subscription   (Followers: 39)
European Respiratory Review     Open Access   (Followers: 7)
Experimental Lung Research     Hybrid Journal   (Followers: 1)
Expert Review of Respiratory Medicine     Hybrid Journal   (Followers: 5)
Heart & Lung: The Journal of Acute and Critical Care     Hybrid Journal   (Followers: 14)
Heart, Lung and Circulation     Full-text available via subscription   (Followers: 9)
Indian Journal of Respiratory Care     Open Access   (Followers: 3)
Indian Journal of Tuberculosis     Full-text available via subscription  
Influenza and Other Respiratory Viruses     Open Access   (Followers: 3)
International Journal of Chronic Obstructive Pulmonary Disease     Open Access   (Followers: 3)
Journal of Association of Chest Physicians     Open Access   (Followers: 2)
Journal of Asthma     Hybrid Journal   (Followers: 5)
Journal of Asthma Allergy Educators     Hybrid Journal   (Followers: 5)
Journal of Bronchology & Interventional Pulmonology     Hybrid Journal   (Followers: 5)
Journal of Clinical Tuberculosis and Other Mycobacterial Diseases     Open Access  
Journal of Heart and Lung Transplantation     Hybrid Journal   (Followers: 12)
Journal of Respiratory Medicine     Open Access   (Followers: 5)
Journal of Respiratory Research     Open Access   (Followers: 2)
Journal of Tuberculosis Research     Open Access   (Followers: 1)
Jurnal Respirasi     Open Access  
Karger Kompass Pneumologie     Full-text available via subscription   (Followers: 1)
Kindheit und Entwicklung     Hybrid Journal  
Lung     Hybrid Journal   (Followers: 3)
Lung Cancer     Hybrid Journal   (Followers: 16)
Lung Cancer International     Open Access   (Followers: 2)
Lung Cancer: Targets and Therapy     Open Access   (Followers: 3)
Lung India     Open Access   (Followers: 1)
Multidisciplinary Respiratory Medicine     Open Access   (Followers: 4)
npj Primary Care Respiratory Medicine     Open Access   (Followers: 2)
Open Journal of Respiratory Diseases     Open Access   (Followers: 2)
Open Respiratory Medicine Journal     Open Access   (Followers: 2)
Paediatric Respiratory Reviews     Hybrid Journal   (Followers: 11)
Pediatric Quality & Safety     Open Access  
Pediatric Respirology and Critical Care Medicine     Open Access   (Followers: 1)
Pulmonary Circulation     Open Access   (Followers: 4)
Pulmonary Medicine     Open Access   (Followers: 3)
Pulmonary Pharmacology & Therapeutics     Hybrid Journal   (Followers: 2)
Pulmonary Therapy     Open Access   (Followers: 2)
Pulmonology and Respiratory Research     Open Access   (Followers: 2)
Respiratory Care     Full-text available via subscription   (Followers: 11)
Respiratory Investigation     Full-text available via subscription   (Followers: 1)
Respiratory Medicine     Hybrid Journal   (Followers: 18)
Respiratory Medicine : X     Open Access  
Respiratory Medicine Case Reports     Open Access  
Respiratory Medicine CME     Hybrid Journal  
Respiratory Medicine Extra     Full-text available via subscription   (Followers: 1)
Respiratory Physiology & Neurobiology     Hybrid Journal   (Followers: 4)
Respiratory Research     Open Access   (Followers: 1)
Respirology     Hybrid Journal   (Followers: 5)
Respirology Case Reports     Open Access  
Revista Americana de Medicina Respiratoria     Open Access  
Revista Chilena de Enfermedades Respiratorias     Open Access  
Revista Inspirar     Open Access  
Revista ORL     Open Access  
Revista Portuguesa de Pneumologia     Open Access  
Sarcoidosis Vasculitis and Diffuse Lung Disese     Full-text available via subscription   (Followers: 3)
Seminars in Respiratory and Critical Care Medicine     Hybrid Journal   (Followers: 14)
Sleep Medicine Reviews     Hybrid Journal   (Followers: 17)
The Clinical Respiratory Journal     Hybrid Journal   (Followers: 3)
The International Journal of Tuberculosis and Lung Disease     Full-text available via subscription   (Followers: 8)
The Lancet Respiratory Medicine     Full-text available via subscription   (Followers: 35)
Therapeutic Advances in Chronic Disease     Open Access   (Followers: 7)
Therapeutic Advances in Respiratory Disease     Open Access   (Followers: 1)
Thorax     Hybrid Journal   (Followers: 38)
Translational Respiratory Medicine     Open Access   (Followers: 1)
Tuberculosis     Hybrid Journal   (Followers: 12)
Tuberculosis Research and Treatment     Open Access   (Followers: 3)
Пульмонология     Full-text available via subscription  


Similar Journals
Journal Cover
Respiratory Physiology & Neurobiology
Journal Prestige (SJR): 0.682
Citation Impact (citeScore): 2
Number of Followers: 4  
  Hybrid Journal Hybrid journal (It can contain Open Access articles)
ISSN (Print) 1569-9048 - ISSN (Online) 1878-1519
Published by Elsevier Homepage  [3203 journals]
  • Inspiratory muscle training improves pulmonary functions and respiratory
           muscle strength in healthy male smokers
    • Abstract: Publication date: June 2019Source: Respiratory Physiology & Neurobiology, Volume 264Author(s): Özgür Bostanci, Hakan Mayda, Coşkun Yılmaz, Menderes Kabadayı, Ali Kerim Yılmaz, Mustafa ÖzdalAbstractThe aim of the present study is to investigate the effects of inspiratory muscle training (IMT) on pulmonary function and respiratory muscle strength of both healthy smokers and nonsmokers. Forty-two healthy males (16 in the IMT smokers group [IMTS], 16 in the IMT nonsmokers group [IMTN], and 10 in the placebo group) participated in the present study. Using a randomized, double-blind, placebo-controlled design, IMTS and IMTN underwent 4 weeks of 30 breaths twice daily at 50% (+5% increase each week) of maximum inspiratory pressure (MIP), while the placebo group maintained 30 breaths twice daily at 15% MIP using an IMT device. The data were analyzed with repeated measures for one-way analysis of variance, 3 × 2 mixed factor analysis of variance, and least significant difference tests. Respiratory muscle strength (MIP and maximal expiratory pressure [MEP]) and pulmonary functions significantly improved after a 4-week period (between the pre and posttests) in the IMTN and IMTS groups (p 
  • Comparison of the CO2 ventilatory response through development in three
           rodent species: Effect of fossoriality
    • Abstract: Publication date: June 2019Source: Respiratory Physiology & Neurobiology, Volume 264Author(s): Ryan J. Sprenger, Anne B. Kim, Yvonne A. Dzal, William K. MilsomAbstractBurrowing rodents have a blunted ventilatory response to CO2 in comparison to non-burrowing rodents. Non-burrowing rats display a period during development where ventilatory responses to hypercarbia become transiently blunted. This study examined the ventilatory responses to CO2 of rats, hamsters and ground squirrels through neonatal development to determine whether the blunted adult response of burrowing species is a retention of the blunting period seen in rats or present from birth. All three species increased ventilation in response to hypercarbia on the day of birth (70–170% in response to 5% CO2; 100–250% in response to 7% CO2). Rats in our study exhibited the triphasic ventilatory response (when expressed as %Δ) to CO2 previously described. In golden-Syrian hamsters, the ventilatory response slowly and progressively waned to a blunted adult response while in the 13-lined ground squirrels, the early ventilatory response to CO2 decreased within days and remained attenuated through development. Our study shows three distinct developmental patterns in the hypercarbic ventilatory response.
  • Exercise energy expenditure in patients with idiopathic pulmonary arterial
           hypertension: impact on clinical severity and survival
    • Abstract: Publication date: Available online 6 April 2019Source: Respiratory Physiology & NeurobiologyAuthor(s): Gabriele Valli, Paolo Palange, Roberto Badagliacca, Silvia Papa, Roberto Poscia, Carmine Dario VizzaAbstractPatient with idiopathic pulmonary hypertension (IPAH) develop peripheral inefficiency which could lead to an increase total energy expenditure and that could have a significant prognostic impact.To test the hypothesis, fifty-five consecutive stable IPAH patients (mean age 51+17 years) and 24 matched controls underwent an incremental exercise test and followed for a 5 years’ period. Total energy expenditure was assessed as the ratio between total VO2 uptake (during both effort and recovery) and total external work (VO2 TOT/WTOT).Patients with IPAH had a lower exercise capacity and a significantly higher VO2 TOT/WTOT than controls ( VO2 TOT/WTOT 0.33 ± 0.09 ml/j vs 0.22 ± 0.04 ml/j, p 
  • Ventilatory Pattern Variability as a Biometric for Severity of Acute Lung
           Injury in Rats
    • Abstract: Publication date: Available online 27 March 2019Source: Respiratory Physiology & NeurobiologyAuthor(s): Benjamin P Young, Kenneth A Loparo, Thomas E Dick, Frank J JaconoAbstractWe hypothesize that ventilatory pattern variability (VPV) varies with the magnitude of acute lung injury (ALI). In adult male rats, we instilled a low- or high- dose of bleomycin or saline (PBS) intratracheally. While representative samples of pulmonary tissue indicated graded lung injury, coefficient of variation (CV) of TTOT did not differ among the 3 groups. Broncho-alveolar lavage fluid (BALF), respiratory rate (fR), mutual information were greater in ALI than sham rats; but did not differ between bleomycin doses. However, nonlinear complexity index (NLCI), which is the difference in sample entropy between original and surrogate data sets was greater for high- versus low- dose; but did not differ between low-dose and sham groups. Further, NLCI correlated to an injury index based on protein concentration of BALF and failure to gain weight. Finally, Receiver Operator Curves (ROCs) indicated that both mutual information and NLCI had greater sensitivity and specificity than fR and CVTTOT in identifying ALI. Thus, nonlinear analyses of VPV can distinguish ALI and out performs fR as a biometric.
  • Targeting progesterone receptors in newborn males and females: From the
           animal model to a new perspective for the treatment of apnea of
    • Abstract: Publication date: May 2019Source: Respiratory Physiology & Neurobiology, Volume 263Author(s): Aida Bairam, Ryma Boukari, Vincent JosephAbstractThe steroid hormone progesterone is well-known for its role in neuroprotection, in the pre- and postnatal brain development, and is also recognized as a potent respiratory stimulant that reduces the frequency of sleep apnea in adult female subjects. Over the past few years, we have used newborn rats or mice to provide convincing evidence that the respiratory effect of progesterone involves a balance between excitation mediated by progesterone receptors, and an inhibition due to the fast conversion of progesterone to allopregnanolone, a positive allosteric modulator of GABAA receptors. This review focuses on the sex- and age- specific roles of nuclear and membrane progesterone receptors (nPR or mPR), and highlight the clinical potential of these receptors for the treatment of apnea of prematurity. We present original data showing that in newborn rats, selective nPR or mPR agonists are more efficient to reduce apnea frequency at postnatal days 12 than at postnatal day 1, and appear more efficient in males than in females. Furthermore, new results obtained by using intra-cisternal injection of specific siRNA targeting mPRα, mPRβ (two mPR with high brain expression) or nPR suggest that mPRβ regulates the stability of the breathing pattern in males, while effects of nPR appear in females. While several important questions remain to be addressed before a safe clinical use could be proposed, these results highlight the potential role of these drugs as complementary, and sex-specific tools for the treatment of apnea in preterm neonates.
  • Mandibular advancement reveals long-term suppression of breathing
           discomfort in patients with obstructive sleep apnea syndrome
    • Abstract: Publication date: May 2019Source: Respiratory Physiology & Neurobiology, Volume 263Author(s): Valérie Attali, Jean-Marc Collet, Olivier Jacq, Sandie Souchet, Isabelle Arnulf, Isabelle Rivals, Jean-Baptiste Kerbrat, Patrick Goudot, Capucine Morelot-Panzini, Thomas SimilowskiAbstractObstructive sleep apnoea syndrome (OSAS) patients do not report breathing discomfort in spite of abnormal upper airway mechanics. We studied respiratory sensations in OSAS patients without and with mandibular advancement device (MAD).Fifty-seven moderate to severe non obese OSAS patients were asked about breathing discomfort using visual analogue scales (VAS) in the sitting position (VAS-1), after lying down (VAS-2), then with MAD (VAS-3). Awake critical closing pressure (awake Pcrit) was measured in 15 patients without then with MAD.None of the patients reported breathing discomfort when sitting but 19 patients (33%) did when lying (VAS-2: -20% or less). A feeling of "easier breathing" with MAD was observed and was more marked in patients reporting breathing discomfort when supine (VAS-3: +66.0% [49.0; 89.0]) than in those not doing so (VAS-3: +28.5% [1.0; 56.5], p = 0.007). MAD-induced change in awake Pcrit was correlated to VAS-3.In conclusion, MAD revealed “latent dyspnea” related to the severity of upper airways mechanics abnormalities in OSAS patients.
  • Inspiratory muscle training improves autonomic modulation and exercise
           tolerance in chronic obstructive pulmonary disease subjects: A
           randomized-controlled trial
    • Abstract: Publication date: May 2019Source: Respiratory Physiology & Neurobiology, Volume 263Author(s): Ana Lídia Carvalho Cutrim, Ana Amélia Machado Duarte, Antonio Carlos Silva-Filho, Carlos José Dias, Christiano Bertoldo Urtado, Rachel Melo Ribeiro, Kátia Rigatto, Bruno Rodrigues, Almir Vieira Dibai-Filho, Cristiano Teixeira MostardaAbstractObjectivesWe aimed to evaluate the effect a regular inspiratory muscle training program on autonomic modulation measured by heart rate variability, exercise capacity and respiratory function in chronic obstructive pulmonary disease subjects (COPD).DesignSingle-center controlled study, with balanced randomization (1:1 for two arms).SettingA COPD reference hospital localized in Sao Luís, Brazil.Participants22 COPD subjects joined the study.InterventionsThree times a week for four weeks inspiratory muscle training (IMT) at 30% of PImax.Main outcome measuresPulmonary capacities and inspiratory pressure, total six-minute walk test and, cardiac autonomic modulation.ResultsThe intervention group showed improvements in the cardiac autonomic modulation, with increased vagal modulation (total variability and HF [ms2; adjusted p 
  • Intercostal muscle blood flow is elevated in old rats during submaximal
    • Abstract: Publication date: May 2019Source: Respiratory Physiology & Neurobiology, Volume 263Author(s): Joshua R. Smith, K. Sue Hageman, Craig A. Harms, David C. Poole, Timothy I. MuschAbstractBackgroundRespiratory muscle blood flows (BF) increase substantially during exercise in younger adult rats. As aging is associated with altered pulmonary function, we hypothesized that old rats will have greater intercostal muscle BF and vascular conductances (VC) than young rats during submaximal exercise.MethodsMean arterial pressure and respiratory muscle BFs (via carotid artery catheter and radiolabeled microspheres, respectively) were measured at rest and during submaximal exercise in young (n = 9) and old (n = 7) Fischer 344 X Brown Norway rats.ResultsAt rest, diaphragm, intercostal, and transversus abdominis BFs and VCs were not different between groups (all, p > 0.10). During submaximal exercise, old compared to young rats had greater intercostal BF (40 ± 6 vs 25 ± 2 mL/min/100 g) and VC (0.30 ± 0.05 vs 0.18 ± 0.02 mL/min/mmHg/100 g) (both, p ≤ 0.01). Diaphragm and transversus abdominis BFs and VCs were not different between groups during exercise (all, p > 0.24).ConclusionsThese data demonstrate that intercostal muscle BF and VC are increased in old compared to young rats during submaximal exercise.
  • TRPM8 channel is involved in the ventilatory response to CO2 mediating
           hypercapnic Ca2+ responses
    • Abstract: Publication date: May 2019Source: Respiratory Physiology & Neurobiology, Volume 263Author(s): Yutaka Hirata, Yoshiro Suzuki, Makoto Tominaga, Yoshitaka OkuAbstractThe role of TRP channels in the ventilatory response to CO2 was investigated in vivo. To this end, the respiration of unrestrained adult TRPM8-, TRPV1- and TRPV4-channel knockout mice was measured using whole-body plethysmography. Under control conditions and hyperoxic hypercapnia, no difference in respiratory parameters was observed between adult wild-type mice and TRPV1- and TRPV4-channel knockout mice. However, TRPM8-channel knockout mice showed decreased tidal volume under both hypercapnia and resting conditions. In addition, the expression of TRPM8, TRPV1 and TRPV4 mRNAs was detected in EGFP-positive glial cells in the medulla of GFAP promoter-EGFP transgenic mice by real-time PCR. Furthermore, we measured intracellular Ca2+ responses of TRPM8-overexpressing HEK-293 cells to hypercapnic acidosis. Subpopulations of cells that exhibited hypercapnic acidosis-induced Ca2+ response also responded to the application of menthol. These results suggest that TRPM8 partially mediates the ventilatory response to CO2 via changes in intracellular Ca2+ and is a chemosensing protein that may be involved in detecting endogenous CO2 production.
  • Transthoracic sonographic assessment of B-line scores during ascent to
           altitude among healthy trekkers
    • Abstract: Publication date: May 2019Source: Respiratory Physiology & Neurobiology, Volume 263Author(s): Rachel Lim, Irene W.Y. Ma, Tom D. Brutsaert, Heidi E. Nysten, Cassandra N. Nysten, Mingma T. Sherpa, Trevor A. DayAbstractSonographic B-lines can indicate pulmonary interstitial edema. We sought to determine the incidence of subclinical pulmonary edema measured by sonographic B-lines among lowland trekkers ascending to high altitude in the Nepal Himalaya. Twenty healthy trekkers underwent portable sonographic examinations and arterial blood draws during ascent to 5160 m over ten days. B-lines were identified in twelve participants and more frequent at 4240 m and 5160 m compared to lower altitudes (P 
  • A simple and safe method for tracheal intubation using a supraglottic
           intubation-aid device in mice
    • Abstract: Publication date: May 2019Source: Respiratory Physiology & Neurobiology, Volume 263Author(s): Hisayo Jin, Takashi Nishino, Tomohiko Aoe, Shiroh IsonoAbstractAlthough mice are a commonly used animal species in experimental medicine, airway management of this species is not easy due to their small size. In order to develop a new method of tracheal intubation in mice, we produced a supraglottic intubation-aid conduit (SIAC) for mice, and tested the efficacy of this device in spontaneously breathing mice anesthetized with sevoflurane inhalation.The success rate of tracheal intubation with the crude prototype of the SIAC was 50% and adverse effects on respiration and some trauma in the upper airway were occasionally observed. After refining the size and shape of the SIAC, the success rate of tracheal intubation with the refined prototype of the SIAC was 100% without any serious adverse effects.This study showed that it is possible to produce a supraglottic airway device to aid tracheal intubation in mice and that the shape and size of the SIAC play a crucial role in successful tracheal intubation in mice.
  • Induction of airway remodeling and persistent cough by repeated citric
           acid exposure in a guinea pig cough model
    • Abstract: Publication date: May 2019Source: Respiratory Physiology & Neurobiology, Volume 263Author(s): Shilei Cui, Isao Ito, Hitoshi Nakaji, Toshiyuki Iwata, Hisako Matsumoto, Tsuyoshi Oguma, Tomoko Tajiri, Tadao Nagasaki, Yoshihiro Kanemitsu, Hiromi Izuhara, Michiaki Mishima, Akio NiimiAbstractBackgroundA previous study involving guinea pigs showed that repeated cough could increase peripheral airway smooth muscle area, which can also aggravate cough. The airway pathologic changes produced by prolonged cough are still unknown.ObjectiveTo study the airway pathologic changes in prolonged cough models of guinea pigs.MethodsGuinea pigs were assigned to three treatment groups: citric acid inhalation (CA) alone, citric acid inhalation with codeine pretreatment (COD), or saline solution inhalation (SA). Animals were challenged with citric acid or saline solution three times weekly. The intervention period was 22 or 43 days. Animals were challenged with citric acid on the first and last days of exposure. Lung specimens were obtained for pathologic analysis 72 h after the last exposure.ResultsCompared with the other two groups, the CA group had increased frequency of cough on both 22 and 43 days of exposure. Tracheal basement membrane (BM) thickness was increased after 43 days of exposure, correlating with the frequency of cough. The area of airway smooth muscles (ASM index) in small airways increased in the CA group after both 22 and 43 days of exposure, compared with the SA group. Compared with the COD group, the ASM index in small airways increased in the CA group after 22 days of exposure instead of 43 days of exposure.ConclusionsAn increase in peripheral smooth muscle area by repeated cough was confirmed. Moreover, this is the first study to show that tracheal BM thickness increased after prolonged exposure (43 days). Repeated cough may lead to airway remodeling, which was also associated with an increased frequency of cough.
  • Central administration of aminooxyacetate, an inhibitor of H2S production,
           affects thermoregulatory but not cardiovascular and ventilatory responses
           to hypercapnia in spontaneously hypertensive rats
    • Abstract: Publication date: May 2019Source: Respiratory Physiology & Neurobiology, Volume 263Author(s): João Paulo J. Sabino, Renato N. Soriano, Bruna M. Santos, Alberto F. Donatti, Rodrigo R. Fernandez, Glauber S.F. da Silva, Luiz G.S. BrancoAbstractHydrogen sulfide (H2S) is classically known for its toxic effects. More recently H2S has been documented as a neuromodulator. Here we investigated the central effects of aminooxyacetate (AOA; inhibitor of the H2S-synthesizing enzyme cystathionine β-synthase, CBS) on cardiovascular, respiratory and thermoregulatory responses to hypercapnia in spontaneously hypertensive rats (SHR). To attain this goal we measured mean arterial pressure (MAP), heart rate (HR), ventilation (VE), and deep body temperature (Tb) of SHR and (normotensive) Wistar Kyoto (WKY) rats before and after microinjection of AOA (9 nmol/μL) or saline into the fourth ventricle immediately followed by 30-min hypercapnia exposure (7% inspired CO2). In saline-treated WKY rats, hypercapnia caused an increase in MAP accompanied by bradycardia, an increase in VE, and a drop in Tb. In AOA-treated WKY rats exposed to hypercapnia, the drug did not affect the increased MAP, potentiated the bradycardic response, attenuated the increased VE, and potentiated the drop in Tb. In saline-treated SHR, in comparison to the saline-treated WKY rats, hypercapnia elicited a minor, shorter-lasting increase in MAP with no changes in HR, evoked a greater increase in VE, and did not induce a drop in Tb. In AOA-treated SHR exposed to hypercapnia, the drug did not change the hypercapnia-induced cardiovascular and ventilatory responses while permitted a drop in Tb. Our findings indicate that AOA, an inhibitor of H2S production, modulates cardiorespiratory and thermoregulatory responses to hypercapnia in normotensive rats, whereas hypertension development in SHR is accompanied by suppression of the AOA effect on the cardiovascular and respiratory responses.
  • MicroRNA-155 regulates lipopolysaccharide-induced mucin 5AC overproduction
           via a suppressor of cytokine signaling 1-mediated mechanism in human
           bronchial epithelial cells
    • Abstract: Publication date: Available online 21 March 2019Source: Respiratory Physiology & NeurobiologyAuthor(s): Chunyi Liu, Xianzhi Du, Xiangdong Zhou, Victor P Kolosov, Juliy M PerelmanAbstractChronic inflammatory lung diseases accompanied by Gram-negative bacteria infection are characterized by excessive mucin production. Lipopolysaccharide (LPS), the major endotoxin released from Gram-negative bacteria, is a potent inflammatory agonist for mucin overproduction. In this study, we sought to examine whether the toll-like receptor (TLR)-responsive microRNA miR-155 plays a role in LPS-provoked induction of mucin 5AC (MUC5AC) and the potential role of suppressor of cytokine signaling 1 (SOCS1) involved in this process. We found that LPS increased the expression of MUC5AC in association with TLR4-dependent miR-155 induction. The suppression of miR-155 by antagomir led to an excessive production of SOCS1, thereby downregulation of MUC5AC production. Collectively, these data imply that miR-155 is involved in LPS-induced MUC5AC overproduction through a TLR4-dependent manner and thereby the downregulation of SOCS1.
  • Minute Ventilation During Hypoxia is Augmented with Capsaicin
           Supplementation in Aged Mice
    • Abstract: Publication date: Available online 21 March 2019Source: Respiratory Physiology & NeurobiologyAuthor(s): Candace N. Receno, Caitlin M. Cunningham, Keith C. DeRuisseau, Lara R. DeRuisseauAbstractCapsaicin is an agonist for transient receptor potential vanilloid 1 (TRPV1), and acute injection results in an increased frequency and tidal volume in young rats. It is unknown how capsaicin influences breathing in aged mice. We tested the hypothesis that capsaicin supplementation would elicit an augmented pattern of breathing in old mice compared to controls. Male 22-month old C57BL/6 J mice consumed a diet containing capsaicin (50 ppm) or lecithin control for one month. Breathing patterns were obtained prior to/following the dietary supplementation period using unrestrained barometric plethysmography. Frequency, tidal volume (VT), minute ventilation (VE), VE to expelled carbon dioxide ratio (VE/VCO2) and VT divided by inspiratory time (VT/Ti) were analyzed at baseline and during a 15-minute hypoxic exposure (10% O2). Capsaicin supplemented mice showed greater VE, VE/VCO2 and TV/Ti during hypoxic exposure compared to controls, with no change at baseline. Overall, these findings suggest an acute augmented response to hypoxia following capsaicin administration in older mice.
  • Development of ventilatory long-term facilitation is dependent on estrous
           cycle stage in adult female rats
    • Abstract: Publication date: Available online 18 March 2019Source: Respiratory Physiology & NeurobiologyAuthor(s): Danielle McIntosh, Brendan J. DoughertyAbstractVentilatory long-term facilitation (vLTF) is a form of respiratory plasticity characterized by a progressive and sustained increase in minute ventilation over time following acute, intermittent hypoxia (AIH). Though vLTF has been repeatedly demonstrated in adult males (rats and humans), few studies have assessed vLTF in adult females and no studies have explored differential expression of vLTF across the normal female estrous cycle. We recently reported that AIH-induced plasticity of phrenic motor output (phrenic long-term facilitation, pLTF), a phenotypically similar form of respiratory plasticity presenting as a sustained increase in phrenic nerve amplitude, develops in adult female rats only during the proestrus stage of the estrous cycle, notable for high levels of serum estrogen. Here, we tested the hypothesis that AIH-induced vLTF would also be estrous-stage dependent; developing in female rats during proestrus, but not estrus. Barometric plethysmography in adult (4-5 months), normally cycling female rats revealed a progressive increase in minute ventilation for 60 min following AIH (5 × 5 min episodes; 10% O2) during proestrus indicative of vLTF, while estrus rats showed no changes in minute ventilation over the same time period. The development of vLTF in proestrus rats was driven by changes in tidal volume production versus respiratory frequency consistent with prior studies. These data are the first to investigate differential vLTF expression across the estrous cycle in adult female rats and highlight the importance of female estrous cycle stage as a critical physiological variable to consider in studies of AIH-induced plasticity.
  • Circulatory control of phrenic motor plasticity
    • Abstract: Publication date: Available online 11 January 2019Source: Respiratory Physiology & NeurobiologyAuthor(s): Raphael R. Perim, Gordon S. MitchellAbstractAcute intermittent hypoxia (AIH) elicits distinct mechanisms of phrenic motor plasticity initiated by brainstem neural network activation versus local (spinal) tissue hypoxia. With moderate AIH (mAIH), hypoxemia activates the carotid body chemoreceptors and (subsequently) brainstem neural networks associated with the peripheral chemoreflex, including medullary raphe serotonergic neurons. Serotonin release and receptor activation in the phrenic motor nucleus then elicits phrenic long-term facilitation (pLTF). This mechanism is independent of tissue hypoxia, since electrical carotid sinus nerve stimulation elicits similar serotonin-dependent pLTF. In striking contrast, severe AIH (sAIH) evokes a spinal adenosine-dependent, serotonin-independent mechanism of pLTF. Spinal tissue hypoxia per se is the likely cause of sAIH-induced pLTF, since local tissue hypoxia elicits extracellular adenosine accumulation. Thus, any physiological condition exacerbating spinal tissue hypoxia is expected to shift the balance towards adenosinergic pLTF. However, since these mechanisms compete for dominance due to mutual cross-talk inhibition, the transition from serotonin to adenosine dominant pLTF is rather abrupt. Any factor that compromises spinal cord circulation will limit oxygen availability in spinal cord tissue, favoring a shift in the balance towards adenosinergic mechanisms. Such shifts may arise experimentally from treatments such as carotid denervation, or spontaneous hypotension or anemia. Many neurological disorders, such as spinal cord injury or stroke compromise local circulatory control, potentially modulating tissue oxygen, adenosine levels and, thus, phrenic motor plasticity. In this brief review, we discuss the concept that local (spinal) circulatory control and/or oxygen delivery regulates the relative contributions of distinct pathways to phrenic motor plasticity.
  • Mechanisms of compensatory plasticity for respiratory motor neuron death
    • Abstract: Publication date: Available online 6 January 2019Source: Respiratory Physiology & NeurobiologyAuthor(s): Yasin B. Seven, Gordon S. MitchellAbstractRespiratory motor neuron death arises from multiple neurodegenerative and traumatic neuromuscular disorders. Despite motor neuron death, compensatory mechanisms minimize its functional impact by harnessing intrinsic mechanisms of compensatory respiratory plasticity. However, the capacity for compensation eventually reaches limits and pathology ensues. Initially, challenges to the system such as increased metabolic demand reveal sub-clinical pathology. With greater motor neuron loss, the eventual result is de-compensation, ventilatory failure, ventilator dependence and then death. In this brief review, we discuss recent advances in our understanding of mechanisms giving rise to compensatory respiratory plasticity in response to respiratory motor neuron death including: 1) increased central respiratory drive, 2) plasticity in synapses on spared phrenic motor neurons, 3) enhanced neuromuscular transmission and 4) shifts in respiratory muscle utilization from more affected to less affected motor pools. Some of these compensatory mechanisms may prolong breathing function, but hasten the demise of surviving motor neurons. Improved understanding of these mechanisms and their impact on survival of spared motor neurons will guide future efforts to develop therapeutic interventions that preserve respiratory function with neuromuscular injury/disease.
  • Probing the function of glycinergic neurons in the mouse respiratory
           network using optogenetics
    • Abstract: Publication date: Available online 3 November 2018Source: Respiratory Physiology & NeurobiologyAuthor(s): Michal G. Fortuna, Sebastian Kügler, Swen HülsmannAbstractGlycine is a primary inhibitory transmitter in the ventral medullary respiratory network, but the functional role of glycinergic neurons for breathing remains a matter of debate. We applied optogenetics to selectively modulate glycinergic neuron activity within regions of the rostral ventral respiratory column (VRC). Responses of the phrenic nerve activity to the light-driven stimulation were studied in the working heart-brainstem preparation from adult glycine transporter 2 Cre mice (GlyT2-Cre), which received a unilateral injection of a Cre-dependent AAV virus into Bötzinger and preBötzinger Complex. Sustained light stimulation from the ventral medullary surface resulted in a substantial depression of the phrenic nerve (PN) frequency, which in most cases was compensated by an increase in PN amplitude. Periodic, burst stimulation with variable intervals could alter and reset respiratory rhythm. We conclude that unilateral activation of the rostral VRC glycinergic neurons can significantly affect respiratory pattern by lengthening the expiratory interval and modulating phase transition.
  • Vive la résistance! The role of inspiratory resistance breathing on
           cerebral blood flow
    • Abstract: Publication date: Available online 16 October 2018Source: Respiratory Physiology & NeurobiologyAuthor(s): Caroline A. RickardsAbstractProlonging the therapeutic window for treatment is imperative for survival from a multitude of life-threatening events such as hemorrhage, cardiac arrest, and stroke. Inspiratory resistance breathing is a therapeutic approach that augments the reduction in intrathoracic and intracranial pressure during inspiration, facilitating improvements in vital organ perfusion under conditions of ischemia, such as blood loss and cardiac arrest. In this review a series of studies will be presented assessing the role of inspiratory resistance breathing on responses of cerebral blood flow and cerebral tissue oxygenation under conditions of cardiac arrest and blood loss in animal models, and simulated hemorrhage in humans. Knowledge gaps in this field of investigation will be presented, and future research directions will be discussed.
  • Pre-phrenic interneurons: Characterization and role in phrenic pattern
           formation and respiratory recovery following spinal cord injury
    • Abstract: Publication date: Available online 10 October 2018Source: Respiratory Physiology & NeurobiologyAuthor(s): Michael George Zaki Ghali, Gavin Britz, Kun-Ze LeeAbstractThe phrenic motor system receives excitatory inspiratory bulbospinal drive from inspiratory pre-motor neurons in the rostral ventral respiratory group and descending inhibition from bulbospinal Bötzinger complex units in the brainstem. While phrenic motoneurons have been extensively studied, a thorough understanding of the role of pre-phrenic interneurons in respiratory pattern formation is only beginning to emerge. Pre-phrenic interneurons are located at upper cervical spinal cord levels, as well as within and around the phrenic nucleus at mid-cervical levels. We speculate they may be involved in polysynaptic bulbospinal relays to phrenic motoneurons and/or may operate independently to modulate respiratory motor outputs. Additionally, pre-phrenic interneurons may serve as a neuroanatomic substrate for a putative spinal respiratory rhythm/pattern generator. Lastly, pre-phrenic interneurons also appear to play an important role in respiratory recovery following spinal cord injury. These various roles subserved by pre-phrenic interneurons are reviewed and discussed.
  • AMPK breathing and oxygen supply
    • Abstract: Publication date: Available online 19 September 2018Source: Respiratory Physiology & NeurobiologyAuthor(s): A. Mark EvansAbstractRegulation of breathing is critical to our capacity to accommodate deficits in oxygen availability and demand during, for example, sleep and ascent to altitude. Key to this are two reflex responses, hypoxic pulmonary vasoconstriction (HPV), which aids ventilation-perfusion matching at the lungs, and the hypoxic ventilatory response (HVR) which accelerates ventilation. In 2004 I proposed that HPV might be mediated by the AMP-activated protein kinase, which governs cell autonomous metabolic homeostasis. Pharmacological evidence was presented in support of this view, and the hypothesis extended to incorporate a role for AMPK in regulating carotid body afferent input responses during hypoxia and thus the HVR. The present article reviews our subsequent findings on these matters and those of others, which provide strong support for the view that AMPK mediates HPV. AMPK is also critical to the HVR, but against our expectations it is not required for carotid body activation during hypoxia. Contrary to current consensus in this respect, our findings suggest that AMPK deficiency blocks the HVR at the level of the brainstem, even when afferent input responses from the carotid body are normal. We have therefore revised our hypothesis on the HVR, now proposing that AMPK integrates local hypoxic stress at defined loci within the brainstem respiratory network with an index of peripheral hypoxic status, namely afferent chemosensory inputs. Nevertheless, in general outcomes are consistent with the original hypothesis, that the role of AMPK has evolved, through natural selection, to extend to the regulation of breathing, and thus oxygen and energy (ATP) supply to the whole body.
  • Acute oxygen sensing—Role of metabolic specifications in peripheral
           chemoreceptor cells
    • Abstract: Publication date: Available online 30 August 2018Source: Respiratory Physiology & NeurobiologyAuthor(s): Lin Gao, Patricia Ortega-Sáenz, José López-BarneoAbstractAcute oxygen sensing is essential for humans under hypoxic environments or pathologic conditions. This is achieved by the carotid body (CB), the key arterial chemoreceptor, along with other peripheral chemoreceptor organs, such as the adrenal medulla (AM). Although it is widely accepted that inhibition of K+ channels in the plasma membrane of CB cells during acute hypoxia results in the activation of cardiorespiratory reflexes, the molecular mechanisms by which the hypoxic signal is detected to modulate ion channel activity are not fully understood. Using conditional knockout mice lacking mitochondrial complex I (MCI) subunit NDUFS2, we have found that MCI generates reactive oxygen species and pyridine nucleotides, which signal K+ channels during acute hypoxia. Comparing the transcriptomes from CB and AM, which are O2-sensitive, with superior cervical ganglion, which is practically O2-insensitive, we have found that CB and AM contain unique metabolic gene expression profiles. The “signature metabolic profile” and their biophysical characteristics could be essential for acute O2 sensing by chemoreceptor cells.
  • Integration of hindbrain and carotid body mechanisms that control the
           autonomic response to cardiorespiratory and glucoprivic insults
    • Abstract: Publication date: Available online 30 August 2018Source: Respiratory Physiology & NeurobiologyAuthor(s): Zohra M. Kakall, E. Myfanwy Cohen, Melissa M.J. Farnham, Seung Jae Kim, Polina E. Nedoboy, Paul M. PilowskyAbstractAutonomic reflex responses are critical in restoring changes to circulatory factors reduced beyond the domain of homeostasis. Intermittent hypoxia triggers repeated activation of chemoreflexes, resulting in baroreflex dysfunction and widespread changes in cellular and neuronal activity regulated by sensory/motor pathways. Hypoglycaemia initiates a rapid neurally-mediated counter-regulatory response. This counter-regulatory response to hypoglycaemia increases plasma adrenaline levels, liver glycogenolysis, and thus blood glucose levels. Context-dependent activation of rostral ventral medullary neurons initiates baroreceptor unloading, peripheral chemoreflex firing and the counter-regulatory response to hypoglycaemia. In this review, we briefly focus on the functional integration between peripheral and medullary pathways comprising the sympathetic baroreflex, chemoreflexes, and the counter-regulatory response to hypoglycaemia.
  • Microglial modulators reduce respiratory rhythm long-term facilitation
           in vitro
    • Abstract: Publication date: Available online 31 July 2018Source: Respiratory Physiology & NeurobiologyAuthor(s): Neira Polet Camacho-Hernández, Jonathan Julio Lorea-Hernández, Fernando Peña-OrtegaAbstractInflammation inhibits the expression of some, but not all forms of respiratory motor plasticity. For example, systemic application of lipopolysaccharide (LPS) inhibits the phrenic long-term facilitation induced by moderate-intermittent hypoxia in vivo. There are multiple pro-inflammatory processes triggered by the systemic application of LPS, including neuroinflammation in the CNS. Considering that microglia can be activated by the systemic application of LPS, it is likely that this cell type influences the response of the respiratory circuits to intermittent hypoxia (IH). Thus, we aimed to test whether modulators of microglial function would affect the response to IH of the preBötzinger complex (preBötC) isolated in a brainstem slice preparation. This experimental approach avoids the systemic influences of these microglial modulators and limits their effects on cells, mostly microglia, included in the slice. First, we found that IH (3 × 5-min episodes of bubbling with 95% N2 and 5% CO2, mixed with 5-min normoxic intervals by bubbling with 95% O2 and 5% CO2) induces a long-lasting increase in the respiratory rhythm frequency recorded directly from the preBötC, called in vitro long-term facilitation (LTF), which occurs simultaneously with a long-lasting decrease in burst amplitude. Moreover, we found that bath applications of “microglial activators” (LPS and fractalkine), “microglial inhibitors” (minocycline and fucoidan) and a microgliotoxin (liposomal clodronate) partially reduce in vitro LTF. These findings reveal a complex scenario in which both the activation and the inhibition of microglia halts IH-induced preBötC plasticity and suggest that experimental or pathological conditions that affect this cell type, almost in any way, could affect breathing and its plastic responses.
  • Modeling hypoglossal motoneurons in the developing rat
    • Abstract: Publication date: Available online 26 July 2018Source: Respiratory Physiology & NeurobiologyAuthor(s): Paul Allen Williams, Clarissa Dalton, Christopher G. WilsonAbstractWe hypothesize that developmental changes in motoneuron volume or surface area in the hypoglossal motor nucleus (XII) can alter the biophysical properties that contribute to motor output. We used the Golgi-Cox technique to stain developing hypoglossal motoneurons (XII MNs) at three postnatal ages (P3, 10, & 17). We removed Sprague-Dawley rat pup brains, processed, sectioned, stained, imaged, and performed 3D reconstructions to quantify the morphometrics of XII MNs. We then used the simulation environment, NEURON, to model the biophysical properties from digitally reconstructed neurons and compared our results to previously published experiments. The total volume of neurons increased from 4766 μ m3 for P3 to 16,904 μ m3 for P17 while the total surface area increased from 4258 μ m2 to 13,510 μ m2 respectively. The P3 simulations required a 10-fold reduction in the hyperpolarization-activated current and doubling of the membrane capacitance to match experimental results. XII MN morphology showed a direct relationship with passive electrophysiological properties and recapitulates the changes seen experimentally.
  • The role of the hypothalamus in modulation of respiration
    • Abstract: Publication date: Available online 19 July 2018Source: Respiratory Physiology & NeurobiologyAuthor(s): Isato Fukushi, Shigefumi Yokota, Yasumasa OkadaAbstractThe hypothalamus is a higher center of the autonomic nervous system and maintains essential body homeostasis including respiration. The paraventricular nucleus, perifornical area, dorsomedial hypothalamus, and lateral and posterior hypothalamus are the primary nuclei of the hypothalamus critically involved in respiratory control. These hypothalamic nuclei are interconnected with respiratory nuclei located in the midbrain, pons, medulla and spinal cord. We provide an extensive review of the role of the above hypothalamic nuclei in the maintenance of basal ventilation, and modulation of respiration in hypoxic and hypercapnic conditions, during dynamic exercise, in awake and sleep states, and under stress. Dysfunction of the hypothalamus causes abnormal breathing and hypoventilation. However, the cellular and molecular mechanisms how the hypothalamus integrates and modulates autonomic and respiratory functions remain to be elucidated.
  • Respiratory fluctuations in pupil diameter are not maintained during
           cognitive tasks
    • Abstract: Publication date: Available online 17 July 2018Source: Respiratory Physiology & NeurobiologyAuthor(s): Nozomu H. Nakamura, Masaki Fukunaga, Yoshitaka OkuAbstractPupil diameter fluctuation throughout the respiratory cycle is autonomically controlled in the resting state, as pupils dilate during inspiration and constrict during expiration. Furthermore, pupil size is differentially modulated by cognitive states between task engagement and disengagement. To determine whether respiratory-dependent fluctuations in pupil size are maintained during a cognitive task, we employed healthy human subjects performing a delayed matching-to-sample task with a short delay and measured their pupil sizes and R wave-to-R wave intervals (RRIs). We detected respiratory fluctuations in pupil size and the RRI during the delay period immediately before the discrimination stage of the task. During the discrimination stage, the cognitive state with the higher task engagement yielded more pupil dilation. However, respiratory fluctuations in pupil size were abolished, whereas those in the RRI were still discernible during the discrimination stage. Our results suggest that an alternative control mechanism involving the cognitive state associated with task engagement overrides the respiratory-related autonomic control of pupil diameter.
  • Astrocyte networks modulate respiration – sniffing glue
    • Abstract: Publication date: Available online 30 June 2018Source: Respiratory Physiology & NeurobiologyAuthor(s): David Forsberg, Eric HerleniusAbstractThe role of astrocytes in the modulation of breathing has emerged. Within the two major respiratory control centers, the inspiration generating preBötzinger Complex and the chemosensitive parafacial respiratory group/retrotrapezoid nucleus, rhythmically active astrocytes have been discovered. These are connected in glial subnetworks that intermingle with the neuronal network. Furthermore, astrocytes modify overall respiratory network behavior through gliotransmitter release, especially during hypoxic and hypercapnic stress. Here, we review some recent discoveries regarding astrocyte-neuronal interactions on a cellular as well as neural network level including the novel gliotransmitter PGE2.
  • No evidence in support of a prodromal respiratory control signature in the
           TgF344-AD rat model of Alzheimer’s disease
    • Abstract: Publication date: Available online 30 June 2018Source: Respiratory Physiology & NeurobiologyAuthor(s): Eric F. Lucking, Kevin H. Murphy, David P. Burns, Anirudh V. Jaisimha, Kevin J. Barry-Murphy, Pardeep Dhaliwal, Barry Boland, Mark G. Rae, Ken D. O’HalloranAbstractAlzheimer’s disease (AD) is a progressive neurodegenerative condition disturbing major brain networks, including those pivotal to the motor control of breathing. The aim of this study was to examine respiratory control in the TgF344-AD transgenic rat model of AD. At 8–11 months of age, basal minute ventilation and ventilatory responsiveness to chemostimulation were equivalent in conscious wild-type (WT) and TgF344-AD rats. Under urethane anesthesia, basal diaphragm and genioglossus EMG activities were similar in WT and TgF344-AD rats. The duration of phenylbiguanide-induced apnoea was significantly shorter in TgF344-AD rats compared with WT. Following bilateral cervical vagotomy, diaphragm and genioglossus EMG responsiveness to chemostimulation were intact in TgF344-AD rats. Amyloid precursor protein C-terminal fragments were elevated in the TgF344-AD brainstem, in the absence of amyloid-β accumulation or alterations in tau phosphorylation. Brainstem pro-inflammatory cytokine concentrations were not increased in TgF344-AD rats. We conclude that neural control of breathing is preserved in TgF344-AD rats at this stage of the disease.
  • Inputs to medullary respiratory neurons from a pontine subregion that
           controls breathing frequency
    • Abstract: Publication date: Available online 28 June 2018Source: Respiratory Physiology & NeurobiologyAuthor(s): Edward J. Zuperku, Astrid G. Stucke, John G. Krolikowski, Jack Tomlinson, Francis A. Hopp, Eckehard A. StuthAbstractNeurons in a subregion of the medial parabrachial (PB) complex control expiratory duration (TE) and the inspiratory on-switch. To better understanding the underlying mechanisms, this study aimed to determine the types of medullary neurons in the rhythmogenic preBötzinger/Bötzinger Complex (preBötC/BötC) and adjacent areas that receive synaptic inputs from the PB subregion and whether these inputs are excitatory or inhibitory in nature. Highly localized electrical stimuli in the PB subregion combined with multi-electrode recordings from respiratory neurons and phrenic nerve activities were used to generate stimulus-to-spike event histograms to detect correlations in decerebrate, vagotomized dogs during isocapnic hyperoxia. Short-time scale correlations were found in 237/442 or ∼54% of the ventral respiratory column (VRC) neurons. Inhibition of E-neurons was ∼2.5X greater than for I-neurons, while Pre-I and I-neurons were excited. These findings indicate that the control of TE and the inspiratory on-switch by the PB subregion are mediated by a marked inhibition of BötC E-neurons combined with an excitation of I-neurons, especially pre-I neurons.
  • The parafacial respiratory group and the control of active expiration
    • Abstract: Publication date: Available online 19 June 2018Source: Respiratory Physiology & NeurobiologyAuthor(s): Annette Pisanski, Silvia PagliardiniAbstractBreathing at rest is typically characterized by three phases: active inspiration, post-inspiration (or stage 1 expiration), and passive expiration (or stage 2 expiration). Breathing during periods of increased respiratory demand, on the other hand, engages active expiration through recruitment of abdominal muscles in order to increase ventilation. It is currently hypothesized that different phases of the respiratory rhythm are driven by three coupled oscillators: the preBötzinger Complex, driving inspiration, the parafacial respiratory group (pFRG), driving active expiration and the post-inspiratory Complex, driving post-inspiration. In this paper we review advances in the understanding of the pFRG and its role in the generation of active expiration across different developmental stages and vigilance states. Recent experiments suggest that the abdominal recruitment varies across development depending on the vigilance state, possibly following the maturation of the network responsible for the generation of active expiration and neuromodulatory systems that influence its activity. The activity of the pFRG is tonically inhibited by GABAergic inputs and strongly recruited by cholinergic systems. However, the sources of these modulatory inputs and the physiological conditions under which these mechanisms are used to recruit active expiration and increase ventilation need further investigation. Some evidence suggests that active expiration during hypercapnia is evoked through disinhibition, while during hypoxia it is elicited through activation of catecholaminergic C1 neurons. Finally, a discussion of experiments indicating that the pFRG is anatomically and functionally distinct from the adjacent and partially overlapping chemosensitive neurons of the retrotrapezoid nucleus is also presented.
  • Breathing with neuromuscular disease: Does compensatory plasticity in the
           motor drive to breathe offer a potential therapeutic target in muscular
    • Abstract: Publication date: Available online 19 June 2018Source: Respiratory Physiology & NeurobiologyAuthor(s): Ken D. O’Halloran, David P. BurnsAbstractDuchenne muscular dystrophy is a fatal neuromuscular disease associated with respiratory-related morbidity and mortality. Herein, we review recent work by our group exploring deficits and compensation in the respiratory control network governing respiratory homeostasis in a pre-clinical model of DMD, the mdx mouse. Deficits at multiple sites of the network provide considerable challenges to respiratory control. However, our work has also revealed evidence of compensatory neuroplasticity in the motor drive to breathe enhancing diaphragm muscle activity during increased chemical drive. The finding may explain the preserved capacity for mdx mice to increase ventilation in response to chemoactivation. Given the profound dysfunction in the primary pump muscle of breathing, we argue that activation of accessory muscles of breathing may be especially important in mdx (and perhaps DMD). Notwithstanding the limitations resulting from respiratory muscle dysfunction, it may be possible to further leverage intrinsic physiological mechanisms serving to compensate for weak muscles in attempts to preserve or restore ventilatory capacity. We discuss current knowledge gaps and the need to better appreciate fundamental aspects of respiratory control in pre-clinical models so as to better inform intervention strategies in human DMD.
  • Swallow-breathing coordination during incremental ascent to altitude
    • Abstract: Publication date: Available online 18 June 2018Source: Respiratory Physiology & NeurobiologyAuthor(s): Alyssa Huff, Trevor A. Day, Mason English, Mitchell D. Reed, Shaelynn Zouboules, Gurkarn Saran, Jack K. Leacy, Carli Mann, Joel D.B. Peltonen, Ken D. O’Halloran, Mingma T. Sherpa, Teresa PittsAbstractSwallow and breathing are highly coordinated behaviors reliant on shared anatomical space and neural pathways. Incremental ascent to high altitudes results in hypoxia/hypocapnic conditions altering respiratory drive, however it is not known whether these changes also alter swallow. We examined the effect of incremental ascent (1045 m, 3440 m and 4371 m) on swallow motor pattern and swallow-breathing coordination in seven healthy adults. Submental surface electromyograms (sEMG) and spirometry were used to evaluate swallow triggered by saliva and water infusion. Swallow-breathing phase preference was different between swallows initiated by saliva versus water. With ascent, saliva swallows changed to a dominate pattern of occurrence during the transition from inspiration to expiration. Additionally, water swallows demonstrated a significant decrease in submental sEMG duration and a shift in submental activity to earlier in the apnea period, especially at 4371 m. Our results suggest that there are changes in swallow-breathing coordination and swallow production that likely increase airway protection with incremental ascent to high altitude. The adaptive changes in swallow were likely due to the exposure to hypoxia and hypocapnia, along with airway irritation.
  • Adrenaline activation of the carotid body: Key to CO2 and pH homeostasis
           in hypoglycaemia and potential pathological implications in cardiovascular
    • Abstract: Publication date: Available online 25 May 2018Source: Respiratory Physiology & NeurobiologyAuthor(s): Andrew P. Holmes, Clare J. Ray, Emma L. Thompson, Ziyad Alshehri, Andrew M. Coney, Prem KumarAbstractVentilatory and neuroendocrine counter-regulatory responses during hypoglycaemia are essential in order to maintain glycolysis and prevent rises in PaCO2 leading to systemic acidosis. The mammalian carotid body has emerged as an important driver of hyperpnoea and glucoregulation in hypoglycaemia. However, the adequate stimulus for CB stimulation in hypoglycaemia has remained controversial for over a decade. The recent finding that adrenaline is a physiological activator of CB in hypoglycaemia raises the intriguing possibility that CB stimulation and hyperpnoea may be necessary to maintain pH in other adrenaline-related hypermetabolic states such as exercise. This review will therefore focus on 1) The important functional contribution of the CB in the counter-regulatory and ventilatory response to hypoglycaemia, 2) the proposed mechanisms that cause CB stimulation in hypoglycaemia including hormonal activation by adrenaline and direct low glucose sensing and 3) the possible pathological consequences of repetitive CB activation by adrenaline that could potentially be targeted to reduce CB-mediated cardiovascular disease.
School of Mathematical and Computer Sciences
Heriot-Watt University
Edinburgh, EH14 4AS, UK
Tel: +00 44 (0)131 4513762

Your IP address:
Home (Search)
About JournalTOCs
News (blog, publications)
JournalTOCs on Twitter   JournalTOCs on Facebook

JournalTOCs © 2009-