Studies Of Airway Smooth Muscle Research Articles

Cyclic GMP-dependent protein kinase regulation of airway smooth muscle in asthma

The mechanisms regulating altered airway smooth muscle (ASM) cell tone and airway reactivity in asthma remain incompletely understood. For vascular smooth muscle (VSM), the most important endogenous relaxation pathway is the nitric oxide (NO)-guanylate cyclase-cyclic GMP-dependent protein kinase type I (PKGI) pathway in which endogenous NO from NO synthases or from exogenous nitrovasodilators activate guanylate cyclase, increasing cGMP levels, and activating PKGI. PKGI in turn targets specific VSM molecules that mediate smooth muscle relaxation. Recent evidence supports that in ASM, like in VSM, activators of guanylyl cyclases have significant cGMP-mediated relaxant and antiproliferative effects. PKGI is therefore a prime but unexplored candidate molecule to mediate ASM relaxation. Recently, we have used mice harbouring a mutation in the leucine zipper N-terminal interaction domain (LZM mice [1]) to test the hypothesis that PKGIα is a critical mediator of ASM relaxation that normally protects against airway hyperresponsivity via interactions with specific molecular targets, including ASM myosin phosphate and Rho/Rho-kinase, and that this regulatory system is perturbed in the setting of asthma. Using this knock-in mouse harboring a discrete mutation in the protein-protein interaction domain of PKGI, which disrupts NO-PKG-mediated smooth muscle relaxation by disrupting the PKGI-myosin phosphatase complex we have begun to explore the mechanism of PKGI-mediated ASM relaxation and the role of PKGI in models of asthma. Several asthma studies in LZM mice and WT littermates have now been performed and analyzed using both the acute and the chronic House Dust Mite (HDM) asthma model in WT and LZM mice. Endpoints examined include airway responsiveness to methacholine; quantification of inflammatory cell populations from Bronchoalveolar lavage (BAL); and studies of airway smooth muscle in the mice. In the LZM mice, there is a significant increase in bronchospasm noted in the airways of mutant mice in both acute and chronic asthma models. No differences between WT and LZM mice in the extent of increase in either total cells or in eosinophilia in BALF samples following HDM was noted in the either the acute or chronic models. The extent and volume of Airway SMC a-actin was also measured in the WT and LZM mice following HDM-induced asthma in the acute model. SMC labeling in the airways was quantified using immunohistochemistry and computerized morphometrics and for each measure, a significant increase in SMC number and total volume was noted in the LZM mice. Studies of PKG expression level and of SMC proliferation in the asthma models are underway. These experiments will provide better understanding of ASM relaxation at the molecular level and have the potential to identify novel gene targets for the development of new therapeutic approaches to bronchoconstriction in asthma.

Methodologic advancements in the study of airway smooth muscle

The study of isolated airway myocytes has provided important information relative to specific processes that regulate contraction, proliferation, and synthetic properties of airway smooth muscle (ASM). To place this information in physiological context, however, improved methods to examine airway biology in vivo are needed. Advances in genetic, biochemical, and optical methods provide unprecedented opportunities to improve our understanding of in vivo physiology and pathophysiology. This article describes 4 important methodologic advances in the study of ASM: (1) the development of transgenic mice that could be used to investigate ASM proliferation and phenotype switching during the development of hypersensitivity, and to investigate excitation-contraction coupling; (2) the use of CD38-deficient mice to confirm the role of CD38-dependent, cyclic adenosine diphosphate-ribose–mediated calcium release in airway responsiveness; (3) investigation of the role of actin filament length and p38 mitogen–activated protein kinase activity in regulating the mechanical plasticity-elasticity balance in contracted ASM; and (d) the use of bronchial biopsies to study ASM structure and phenotype in respiratory science

Bases physiologiques de l'utilisation des antagonistes muscariniques dans les dysplasies bronchopulmonaires

The rationale for the use of muscarinic antagonists in bronchopulmonary dysplasia (BPD) is based on the physiology and pharmacology of airway smooth muscle, the pathology of BPD, and the response of infants with BPD to bronchodilators, in vivo and in vitro studies of airway smooth muscle of newborn animals and humans indicate that vagal efferent airway innervation and/or muscarinic receptors are functional at birth, as well as early in gestation. Current concepts regarding muscarinic receptor subtypes suggest that M3 receptors mediate airway smooth muscle contraction, M2 receptors are autoinhibitory and limit vagally-mediated bronchoconstriction, and M1 receptors may play a facilitatory role in ganglionic transmission. Muscarinic receptor subtypes appear to be functionally expressed at birth but may undergo developmental regulation. Infants with BPD have an elevated pulmonary resistance that is accompanied by hypertrophy of airway smooth muscle, b2-agonists cause bronchodilation in BPD as does atropine in infants recovering from severe BPD. The synthetic congener of atropine, ipratropium bromide (IPB) causes bronchodilation in ventilator-dependent infants with BPD in a dose-dependent fashion. Nebulized IPB causes a decrease in respiratory resistance that reaches a maximum of 20% at 175 mg. The bronchodilation seen with muscarinic antagonists suggests that part of the elevated resistance associated with BPD is due to increased muscarinic tone, presumably vagal in origin. When IPB is combined with salbutamol (0.04 mg) the response is increased in magnitude and duration; reaching a slightly larger decreases in resistance (26%) that is now accompanied by an increase in compliance (20%).(ABSTRACT TRUNCATED AT 250 WORDS)

Use of cultured airway myocytes for study of airway smooth muscle

Cultured airway smooth muscle cells provide a convenient model system for studying the regulation of a wide range of airway responses at the cellular level. This review describes the characteristics of cultured airway smooth muscle cells and differences that exist between cultured cells and acutely dissociated cells or muscle strips. Receptor and ion-channel expression and control of coupling in cultured airway smooth muscle are reviewed. The methodology for airway smooth muscle culture is discussed. The main advantage of using cultured airway smooth muscle cells is that studies can be performed to examine long-term control of cell responses. Studies of the regulation of receptor expression and coupling, desensitization of receptor or channel-mediated responses, or regulation of the expression of important enzymes or muscle proteins can be readily performed in cell culture. In addition, cultured airway myocytes provide a useful secondary screening system for the development of novel therapeutic agents targeted at airway receptors that are expressed upon these cells.

Airway Smooth Muscle Mechanics and Biochemistry in Experimental Asthma

Introduction Asthma research seems to be entering the doldrums; there is much fine-tuning but no real breakthroughs. Certainly nothing approaching the drama of the cystic fibrosis story is anywhere on the asthma scene. We still do not have a clear-cut mechanism for the pathogenesis of asthma, and we still seem unwilling to direct attention toward primary causes. Although this certainly applies to the area of airway smooth muscle mechanics, it is not true for other areas of airway research such as inflammation in the pathogenesis of bronchial hyperreactivity. In our laboratory, research seems remote from primary causes and concerned less with the pathogenesis of asthma and more with elucidation of physiologic regulation of airway smooth muscle contraction. Just how long we can pursue this approach is moot; the urgency of the times, goaded by the increasing incidence of asthma, demands that more immediate attention be paid to applied research. The above points notwithstanding, what we propose to do is to describe some of the physiologic data we have recently obtained and attempt to relate these to what may be occurring in animal models of allergic or inbred hyperreactivity that we have studied (1). The material in this chapter will deal with the following. 1. The development of the bronchial smooth muscle preparation for study of the mechanical properties of those airway smooth muscles that are directly involved in allergic bronchospasm. 2. The importance of structural studies of airway smooth muscle in understanding regional regulation of ventilation and allergic bronchoconstriction. 3. The development of a rat model of inbred hyperreactivity of airway smooth muscle. 4. Mechanism of the increased velocity of shortening that is seen in antigen-sensitized airway smooth muscle. Finally, an apology must be offered for our not adhering to the editor's injunction of comparing the mechanical properties' of airway smooth muscle from asthmatics and chronic obstructive pulmonary disease. The reader is referred to other sections in the supplement for this.

Workshop on airway smooth muscle. Summary of a conference held September 25-27 1983.

Airway smooth muscle contraction and the extreme sensitivity of the airway smooth muscle responses to various stimuli are accepted as key factors in the pathogenesis of asthma and are recognized to be important in other diseases (e.g., bronchitis and cystic fibrosis). A Workshop on Airway Smooth Muscle sponsored by the National Heart, Lung and Blood Institute (September 25 to 27, 1983) identified various avenues of future research. Smooth muscle anatomists pointed to the paucity of quantitative information on airway smooth muscle structure, especially electron microscopic information and details of the neural arrangement. Investigations of the neural network, similar to those that have led to important discoveries in the gut, are urgently needed. Now that intramural ganglia can be studied electrophysiologically (and in vivo!), new information concerning possible local neural modulation can be examined. A similar lack of information was found in the biochemical study of airway smooth muscle. Among potential causes of abnormalities in asthmatic muscles are alterations in membrane channels and pumps, receptor transduction processes, cGMP-mediated processes, and other metabolic pathways. Inflammation and inflammatory mediators appear to play important roles in disease of airway smooth muscle. Utilization of cell isolation and culture, and immunologic and other cell biologic and biochemical methods will accelerate the study of the various cells in the airways, their interactions, and their roles in disease. Of special potential importance are peptide and lipid mediators produced by various airway cells. Development of synthetic analogues and antagonists, including monoclonal antibodies, will provide more specific tools for dissecting these cell-to-cell interactions. Regardless of the level of study--from examination of the whole organism to molecular mechanisms--the fact is that there is no entirely satisfactory animal "model" of asthma or asthmatic muscle, presumably because we do not fully understand the etiology and pathogenesis of asthma. This makes it all the more important to take appropriate opportunities to obtain tissue from asthmatics for laboratory study. Relatively simple, careful studies of asthmatic smooth muscle may prove important, unique insights into its possible abnormalities.

Slow-reacting substances (leukotrienes) contract human airway and pulmonary vascular smooth muscle in vitro.

During a type I allergic reaction histamine, slow-reacting substance of anaphylaxis (SRS-A) and other mediator substances are elaborated from specific tissue sites. In allergic asthma these sites are in the lung and the mediator substances cause airway obstruction by contracting smooth muscle and altering mucociliary function. Unlike histamine, slow-reacting substances (SRSs) have been assessed very little for their roles in obstructive airways disease. This has been partly due to the fact that their chemical nature was unknown until recently and thus pure samples were not available for pharmacological studies. However, SRSs isolated from both immunological and non-immunological reactions have been identified as a combination of two related lipid substances--leukotriene C4 (LTC) and leukotriene D4 (LTD); thus it is now possible to use pure SRSs (leukotrienes) in pharmacological studies of airway smooth muscle. LTC and LTD have been shown to contract guinea pig tracheal and lung parenchymal strips but there is no evidence that these substances produce similar effects on human lung tissue. To clarify this, in vivo pharmacological studies were done to determine the actions of LTC and LTD on smooth muscle strips of human bronchus, pulmonary vein and artery, and lung parenchymal tissue containing smooth muscle components and pleura. As indicated in a preliminary report, all four types of tissues contracted in a dose-dependent fashion to the leukotrienes, although these substances only function as partial agonists.

Pharmacological modulation of cholinergic neurotransmission in guinea pig trachea in vitro

Electrical (field) stimulation of the isolated guinea pig trachea with normal intrinsic tone produced a biphasic response which consisted of an initial (cholinergic) contraction followed by (adrenergic and nonadrenergic) relaxation. Treatment of the tissue with the prostaglandin synthetase inhibitor indomethacin (2.8–5.6 μM) removed intrinsic tone and increased the responsiveness of the tissue to stimulation of cholinergic nerves and to exogenous acetylcholine. Indomethacin-relaxed tracheae were subsequently used to study cholinergic neurotransmission because under these experimental conditions only the contractile component of the response to electrical stimulation was observed. The β adrenoceptor blocking agents dl-propranolol and sotalol and the adrenergic neuron blocking agent guanethidine produced further enhancement of the contraction to electrical stimulation at low frequency (1–10 Hz). Prostaglandin E1, l-noradrenaline, l-adrenaline, salbutamol, phenylephrine, and phentolamine selectively attenuated the contractions to electrical stimulation in concentrations which did not significantly alter the matched responses to exogenous acetylcholine. The selective depressant effect of l-noradrenaline, l-adrenaline, salbutamol, phenylephrine, and phentolamine but not prostaglandin E1 were blocked by dl-propranolol or sotalol. The present results demonstrate that responses to stimulation of cholinergic nerves were altered by (1) prostaglandins and inhibitors of their synthesis, (2) neurally released adrenergic transmitter, and (3) exogenously added β adrenoceptor agonists. The possibility that prostaglandins and adrenergic neurotransmitter may modulate cholinergic neurotransmission at both pre- and post-junctional sites is hypothesized. It is proposed that more attention should be paid to the role of cholinergic transmission and its modulation in the studies of airway smooth muscle.

Methods of study of airway smooth muscle and its physiology

Methods of study of airway smooth muscle and its physiology

Test of wave-speed theory of flow limitation in elastic tubes.

ARTICLESTest of wave-speed theory of flow limitation in elastic tubesE. A. Elliott, and S. V. DawsonE. A. Elliott, and S. V. DawsonPublished Online:01 Sep 1977https://doi.org/10.1152/jappl.1977.43.3.516MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByMimicking a flow-limited human upper airway using a collapsible tube: relationships between flow patterns and pressures in a respiratory modelKaixian Zhu, Ramon Farré, Ira Katz, Sébastien Hardy, and Pierre Escourrou22 August 2018 | Journal of Applied Physiology, Vol. 125, No. 2Relation of concavity in the expiratory flow-volume loop to dynamic hyperinflation during exercise in COPDRespiratory Physiology & Neurobiology, Vol. 234State-dependent and reflex drives to the upper airway: basic physiology with clinical implicationsRichard L. Horner, Stuart W. Hughes, and Atul Malhotra*1 February 2014 | Journal of Applied Physiology, Vol. 116, No. 3Liquid VentilationTotal Liquid Ventilation: Dynamic Airway Pressure and the Development of Expiratory Flow LimitationASAIO Journal, Vol. 50, No. 5Assessment of the development of choked flow during total liquid ventilationCritical Care Medicine, Vol. 32, No. 1The Male Predisposition to Pharyngeal CollapseAmerican Journal of Respiratory and Critical Care Medicine, Vol. 166, No. 10Mechanical properties of the passive pharynx in Vietnamese pot-bellied pigs. I. StaticsStephanie A. Tuck, and John E. Remmers1 June 2002 | Journal of Applied Physiology, Vol. 92, No. 6Mechanical properties of the passive pharynx in Vietnamese pot-bellied pigs. II. DynamicsStephanie A. Tuck, and John E. Remmers1 June 2002 | Journal of Applied Physiology, Vol. 92, No. 6Interdependence of flow between lobes reduces maximal emptying postresection in dogsDavid Ewing-Bui, and Steven N. Mink1 January 2002 | Journal of Applied Physiology, Vol. 92, No. 1Gender Differences in the Expression of Sleep-Disordered BreathingChest, Vol. 120, No. 5Modeling expiratory flow from excised tracheal tube lawsNikolai Aljuri, Lutz Freitag, and José G. Venegas1 November 1999 | Journal of Applied Physiology, Vol. 87, No. 5Effect of expiratory flow limitation on respiratory mechanical impedance: a model studyR. Peslin, R. Farré, M. Rotger, and D. Navajas1 December 1996 | Journal of Applied Physiology, Vol. 81, No. 6Air trapping in the lungs during cardiopulmonary resuscitation in dogs. A mechanism for generating changes in intrathoracic pressure.Circulation Research, Vol. 65, No. 4The effects of wall thickness, axial strain and end proximity on the pressure-area relation of collapsible tubesJournal of Biomechanics, Vol. 20, No. 9A consideration of density dependence of maximum expiratory flowRespiration Physiology, Vol. 52, No. 1Methods of study of airway smooth muscle and its physiologyPharmacology & Therapeutics, Vol. 7, No. 2 More from this issue > Volume 43Issue 3September 1977Pages 516-522 Copyright & PermissionsCopyright © 1977 the American Physiological Societyhttps://doi.org/10.1152/jappl.1977.43.3.516PubMed914722History Published online 1 September 1977 Published in print 1 September 1977 Metrics

Effect of changing airway mechanics on maximum expiratory flow.

ARTICLESEffect of changing airway mechanics on maximum expiratory flowJ. G. Jones, R. B. Fraser, and J. A. NadelJ. G. Jones, R. B. Fraser, and J. A. NadelPublished Online:01 Jun 1975https://doi.org/10.1152/jappl.1975.38.6.1012MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmailWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformationCited ByInteraction of cross-sectional area, driving pressure, and airflow of passive velopharynxShiroh Isono, Thom R. Feroah, Eric A. Hajduk, Rollin Brant, William A. Whitelaw, and John E. Remmers1 September 1997 | Journal of Applied Physiology, Vol. 83, No. 3Anatomy of pharynx in patients with obstructive sleep apnea and in normal subjectsShiroh Isono, John E. Remmers, Atsuko Tanaka, Yasuhide Sho, Jiro Sato, and Takashi Nishino1 April 1997 | Journal of Applied Physiology, Vol. 82, No. 4Methods of study of airway smooth muscle and its physiologyPharmacology & Therapeutics, Vol. 7, No. 2 More from this issue > Volume 38Issue 6June 1975Pages 1012-1021 Copyright & PermissionsCopyright © 1975 the American Physiological Societyhttps://doi.org/10.1152/jappl.1975.38.6.1012PubMed1141113History Published online 1 June 1975 Published in print 1 June 1975 Metrics

Time dependence of flow-volume curves.

Time dependence of flow-volume curves.

Influence of constriction in central or peripheral airways on maximal expiratory flow rates in dogs.

ARTICLESInfluence of constriction in central or peripheral airways on maximal expiratory flow rates in dogsA. J. Gardiner, L. Wood, P. Gayrard, H. Menkes, and P. MacklemA. J. Gardiner, L. Wood, P. Gayrard, H. Menkes, and P. MacklemPublished Online:01 May 1974https://doi.org/10.1152/jappl.1974.36.5.554MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByCommentary on “The role of the large airways on smooth muscle contraction in asthma”Peter Macklem1 October 2007 | Journal of Applied Physiology, Vol. 103, No. 4Assessment of the development of choked flow during total liquid ventilationCritical Care Medicine, Vol. 32, No. 1Partitioning of pulmonary resistance in Friesian calvesResearch in Veterinary Science, Vol. 42, No. 3Methods of study of airway smooth muscle and its physiologyPharmacology & Therapeutics, Vol. 7, No. 2 More from this issue > Volume 36Issue 5May 1974Pages 554-560 Copyright & PermissionsCopyright © 1974 the American Physiological Societyhttps://doi.org/10.1152/jappl.1974.36.5.554PubMed4826318History Published online 1 May 1974 Published in print 1 May 1974 Metrics

Pressure-flow relationships in the isolated canine trachea.

ArticlePressure-flow relationships in the isolated canine trachea.R J Knudson, and D E KnudsonR J Knudson, and D E KnudsonPublished Online:01 Dec 1973https://doi.org/10.1152/jappl.1973.35.6.804MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByExcessive Dynamic Airway Collapse: Fact, Fiction, or Flow LimitationAnnals of the American Thoracic Society, Vol. 14, No. 2Test of the Starling resistor model in the human upper airway during sleepAndrew Wellman, Pedro R. Genta, Robert L. Owens, Bradley A. Edwards, Scott A. Sands, Stephen H. Loringhttp://orcid.org/0000-0002-6277-3979, David P. White, Andrew C. Jackson, Ole F. Pedersenhttp://orcid.org/0000-0002-1153-3844, and James P. Butler15 December 2014 | Journal of Applied Physiology, Vol. 117, No. 12Expiratory Flow Limitation1 October 2011Modeling expiratory flow from excised tracheal tube lawsNikolai Aljuri, Lutz Freitag, and José G. Venegas1 November 1999 | Journal of Applied Physiology, Vol. 87, No. 5Effect of hypercapnia on upper airway resistance and collapsibility in anesthetized dogsRespiration Physiology, Vol. 75, No. 1Experimental and theoretical models of flow during forced expiration: pressure and pressure history dependence of flow rateMedical & Biological Engineering & Computing, Vol. 25, No. 5Methods of study of airway smooth muscle and its physiologyPharmacology & Therapeutics, Vol. 7, No. 2Biomechanical Characteristics of the Canine Trachea29 June 2016 | Annals of Otology, Rhinology & Laryngology, Vol. 87, No. 4 More from this issue > Volume 35Issue 6December 1973Pages 804-12 https://doi.org/10.1152/jappl.1973.35.6.804PubMed4765815History Published online 1 December 1973 Published in print 1 December 1973 Metrics

Comparison of esophageal and pleural pressures in the anesthetized dog.

ArticleComparison of esophageal and pleural pressures in the anesthetized dog.D J Gillespie, Y L Lai, and R E HyattD J Gillespie, Y L Lai, and R E HyattPublished Online:01 Nov 1973https://doi.org/10.1152/jappl.1973.35.5.709MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformationCited ByThoracic gas compression during forced expiration is greater in men than womenPhysiological Reports, Vol. 8, No. 6Automated expiratory ventilation assistance through a small endotracheal tube can improve venous return and cardiac output9 January 2019 | Intensive Care Medicine Experimental, Vol. 7, No. 1Reliability of transpulmonary pressure–time curve profile to identify tidal recruitment/hyperinflation in experimental unilateral pleural effusion20 July 2016 | Journal of Clinical Monitoring and Computing, Vol. 31, No. 4Transpulmonary Pressure Meaning: Babel or Conceptual Evolution?American Journal of Respiratory and Critical Care Medicine, Vol. 195, No. 10Correcting the dynamic response of a commercial esophageal balloon-catheterTroy J. Cross, Kenneth C. Beck, and Bruce D. Johnson9 August 2016 | Journal of Applied Physiology, Vol. 121, No. 2Response characteristics of esophageal balloon catheters handmade using latex and nonlatex materials15 June 2015 | Physiological Reports, Vol. 3, No. 6Comparative Ventilation of the Normal LungThe assessment of transpulmonary pressure in mechanically ventilated ARDS patients12 August 2014 | Intensive Care Medicine, Vol. 40, No. 11Compressive Forces and Computed Tomography–derived Positive End-expiratory Pressure in Acute Respiratory Distress SyndromeAnesthesiology, Vol. 121, No. 3Pleural Effusion in Patients With Acute Lung InjuryCritical Care Medicine, Vol. 41, No. 4Propofol Attenuates the Decrease of Dynamic Compliance and Water Content in the Lung by Decreasing Oxidative Radicals Released from the Reperfused LiverAnesthesia & Analgesia, Vol. 107, No. 4Lung Stress and Strain during Mechanical Ventilation for Acute Respiratory Distress SyndromeAmerican Journal of Respiratory and Critical Care Medicine, Vol. 178, No. 4Telemetric Recording of Intrapleural PressureJournal of Surgical Research, Vol. 138, No. 1Novel aspects of pulmonary mechanics in intensive careBritish Journal of Anaesthesia, Vol. 91, No. 1A novel method for chronic measurement of respiratory function in the conscious monkeyJournal of Pharmacological and Toxicological Methods, Vol. 46, No. 1Recruitment and Derecruitment During Acute Respiratory FailureAmerican Journal of Respiratory and Critical Care Medicine, Vol. 164, No. 1Lung and Chest Wall Mechanics in Anesthetized ChildrenAmerican Journal of Respiratory and Critical Care Medicine, Vol. 162, No. 2A novel method for chronic measurement of pleural pressure in conscious ratsJournal of Pharmacological and Toxicological Methods, Vol. 39, No. 3Assessment of Pulmonary Function and the Effects of Inhaled Toxicants12 July 2013Was it just our problem, or yours too? errors in body plethysmography, in infants, children, and adultsPediatric Pulmonology, Vol. 11, No. 4Mechanical Heart-Lung Interaction in the Adult Respiratory Distress SyndromeClinics in Chest Medicine, Vol. 11, No. 4Effects of Mechanical Ventilation on Right and Left Ventricular FunctionClinics in Chest Medicine, Vol. 9, No. 1A critical assessment of pulmonary function testing in exercising poniesVeterinary Research Communications, Vol. 12, No. 1Ventilation: Total, Alveolar, and Dead Space1 January 2011Effects of intravenous atropine on static P-V curves of the lung in normal manRespiration Physiology, Vol. 70, No. 2Drug-Induced Effects on Reticular Groove Reflex, Eructation and RuminationEffects of intravenous atropine on static P-V curves of the lung in normal manRespiration Physiology, Vol. 70, No. 1Tests of Mechanical Function1 January 2011Methods of study of airway smooth muscle and its physiologyPharmacology & Therapeutics, Vol. 7, No. 2Physiologic Effects of the Position of the Body in Experimental Unilateral EmphysemaChest, Vol. 74, No. 1 More from this issue > Volume 35Issue 5November 1973Pages 709-13 https://doi.org/10.1152/jappl.1973.35.5.709PubMed4770355History Published online 1 November 1973 Published in print 1 November 1973 Metrics

Transvenous phrenic nerve stimulation in anesthetized dogs.

ArticleTransvenous phrenic nerve stimulation in anesthetized dogs.A Wanner, and M A SacknerA Wanner, and M A SacknerPublished Online:01 Apr 1973https://doi.org/10.1152/jappl.1973.34.4.489MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByMapping for Acute Transvenous Phrenic Nerve Stimulation Study (MAPS Study)14 February 2017 | Pacing and Clinical Electrophysiology, Vol. 40, No. 3Transvenous versus perinervous stimulation of the phrenic nerve to assess the diaphragmatic strength in rabbitsJournal of Neuroscience Methods, Vol. 76, No. 2Respiratory Sinus ArrhythmiaCirculation, Vol. 94, No. 4Effects of bilateral transvenous diaphragm pacing on hemodynamic function in patients after cardiac operationsThe Journal of Thoracic and Cardiovascular Surgery, Vol. 100, No. 1Effects of brief and intermediate exposures to sulfate submicron aerosols and sulfate injections on cardiopulmonary function of dogs and tracheal mucous velocity of sheep20 October 2009 | Journal of Toxicology and Environmental Health, Vol. 7, No. 6Cardiopulmonary effects of short-term nitrogen dioxide exposure in conscious sheepEnvironmental Research, Vol. 22, No. 1Methods of study of airway smooth muscle and its physiologyPharmacology & Therapeutics, Vol. 7, No. 2Diaphragm pacingThe Journal of Thoracic and Cardiovascular Surgery, Vol. 74, No. 1Effect of Beta-Adrenergic Agonists Aerosolized by Freon Propellant on Tracheal Mucous Velocity and Cardiac OutputChest, Vol. 69, No. 5Effect of Oxygen in Graded Concentrations upon Tracheal Mucous VelocityChest, Vol. 69, No. 2Effect of Cuffed Endotracheal Tubes on Tracheal Mucous VelocityChest, Vol. 68, No. 6Pulmonary Arterial Blood Volume and Tissue Volume in Man and DogCirculation Research, Vol. 34, No. 6Pathogenesis and Prevention of Tracheobronchial Damage with Suction ProceduresChest, Vol. 64, No. 3 More from this issue > Volume 34Issue 4April 1973Pages 489-94 https://doi.org/10.1152/jappl.1973.34.4.489PubMed4698606History Published online 1 April 1973 Published in print 1 April 1973 Metrics

Pulmonary conductance and elastic recoil relationships in asthma and emphysema.

Pulmonary conductance and elastic recoil relationships in asthma and emphysema.

Glottis opening and airway resistance.

Glottis opening and airway resistance.

Bronchial closure with Mecholyl in excised dog lobes.

ArticleBronchial closure with Mecholyl in excised dog lobes.P S Murtagh, D F Proctor, S Permutt, B Kelly, and S EveringP S Murtagh, D F Proctor, S Permutt, B Kelly, and S EveringPublished Online:01 Sep 1971https://doi.org/10.1152/jappl.1971.31.3.409MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByIt's Not All Smooth Muscle: Non-Smooth-Muscle Elements in Control of Resistance to AirflowAnnual Review of Physiology, Vol. 72, No. 1The role of the large airways on smooth muscle contraction in asthmaSolbert Permutt1 October 2007 | Journal of Applied Physiology, Vol. 103, No. 4Effects of chest wall strapping on mechanical response to methacholine in humansRoberto Torchio, Carlo Gulotta, Claudio Ciacco, Alberto Perboni, Marco Guglielmo, Flavio Crosa, Mario Zerbini, Vito Brusasco, Robert E. Hyatt, and Riccardo Pellegrino1 August 2006 | Journal of Applied Physiology, Vol. 101, No. 2The structural basis of airways hyperresponsiveness in asthmaRobert H. Brown, David B. Pearse, George Pyrgos, Mark C. Liu, Alkis Togias, and Solbert Permutt1 July 2006 | Journal of Applied Physiology, Vol. 101, No. 1Invited Review: Understanding airway pathophysiology with computed tomograpyRobert H. Brown, and Wayne Mitzner1 August 2003 | Journal of Applied Physiology, Vol. 95, No. 2Methacholine-Induced Temporal Changes in Airway Geometry and Lung Density by CTChest, Vol. 119, No. 6High-Resolution Computed Tomographic Evaluation of Airway Distensibility and the Effects of Lung Inflation on Airway Caliber in Healthy Subjects and Individuals with AsthmaAmerican Journal of Respiratory and Critical Care Medicine, Vol. 163, No. 4Effect of transpulmonary pressure on airway diameter and responsiveness of immature and mature rabbitsX. Shen, R. Ramchandani, B. Dunn, R. Lambert, S. J. Gunst, and R. S. Tepper1 October 2000 | Journal of Applied Physiology, Vol. 89, No. 4Potent bronchoprotective effect of deep inspiration and its absence in asthmaTrisevgeni Kapsali, Solbert Permutt, Beth Laube, Nicola Scichilone, and Alkis Togias1 August 2000 | Journal of Applied Physiology, Vol. 89, No. 2Differences in Airway Closure between Normal and Asthmatic Subjects Measured with Single-Photon Emission Computed Tomography and TechnegasAmerican Journal of Respiratory and Critical Care Medicine, Vol. 158, No. 6PhysiologyNEW TECHNIQUES AND DEVELOPMENTS IN PHYSIOLOGIC IMAGING OF AIRWAYSRadiologic Clinics of North America, Vol. 36, No. 1Interaction between airway edema and lung inflation on responsiveness of individual airways in vivoRobert H. Brown, Wayne Mitzner, and Elizabeth M. Wagner1 August 1997 | Journal of Applied Physiology, Vol. 83, No. 2Effect of lung inflation in vivo on airways with smooth muscle tone or edemaRobert H. Brown, Wayne Mitzner, Yonca Bulut, and Elizabeth M. Wagner1 February 1997 | Journal of Applied Physiology, Vol. 82, No. 2The relevance of pharmacological dose—response curves to airway narrowingTrends in Pharmacological Sciences, Vol. 10, No. 12Bronchial HyporesponsivenessChest, Vol. 91, No. 6Bronchial HyporesponsivenessChest, Vol. 87, No. 5Influence of lung inflation on the elastic properties of intra- and extrapulmonary airways in manRespiration Physiology, Vol. 37, No. 3Methods of study of airway smooth muscle and its physiologyPharmacology & Therapeutics, Vol. 7, No. 2Relation Between Pulmonary Arterial Pressure and Pleural Pressure During the Acute Asthmatic AttackChest, Vol. 63, No. 4 More from this issue > Volume 31Issue 3September 1971Pages 409-15 https://doi.org/10.1152/jappl.1971.31.3.409PubMed5111859History Published online 1 September 1971 Published in print 1 September 1971 Metrics

Constriction of isolated living liquid-filled dog and cat lungs with histamine.

ArticleConstriction of isolated living liquid-filled dog and cat lungs with histamine.H J Colebatch, and C A MitchellH J Colebatch, and C A MitchellPublished Online:01 May 1971https://doi.org/10.1152/jappl.1971.30.5.691MoreSectionsPDF (3 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByCommunications between Pulmonary Airways and Blood Vessels. A New Mechanism?American Journal of Respiratory and Critical Care Medicine, Vol. 196, No. 7The Use of Silicone Casts in Collection of Morphological Data from Free-Ranging Wildlife — the Case of Tracheobronchial Anatomy of the Eurasian Lynx ( Lynx lynx )Annales Zoologici Fennici, Vol. 50, No. 5Biophysical basis for airway hyperresponsivenessThis article is one of a selection of papers published in the Special Issue on Recent Advances in Asthma Research.Canadian Journal of Physiology and Pharmacology, Vol. 85, No. 7COUNTERPOINT: AIRWAY SMOOTH MUSCLE IS NOT USEFULJeffrey J. Fredberg1 April 2007 | Journal of Applied Physiology, Vol. 102, No. 4Bronchospasm and its biophysical basis in airway smooth muscle26 February 2004 | Respiratory Research, Vol. 5, No. 1Nonlinearity of respiratory mechanics during bronchoconstriction in mice with airway inflammationScott Wagers, Lennart Lundblad, Henrique T. Moriya, Jason H. T. Bates, and Charles G. Irvin1 May 2002 | Journal of Applied Physiology, Vol. 92, No. 5Historical perspective on airway smooth muscle: the saga of a frustrated cellC. Y. Seow, and J. J. Fredberg1 August 2001 | Journal of Applied Physiology, Vol. 91, No. 2α-Actin: disposition, quantities, and estimated effects on lung recoil and complianceE. H. Oldmixon, K. Carlsson, C. Kuhn, J. P. Butler, and F. G. Hoppin1 July 2001 | Journal of Applied Physiology, Vol. 91, No. 1Effects of smooth muscle activation on axial mechanical properties of excised canine bronchiFelix R. Shardonofsky, Todd M. Officer, Aladin M. Boriek, and Joseph R. Rodarte1 April 2001 | Journal of Applied Physiology, Vol. 90, No. 4Eglin-c prevents monocrotaline-induced ventilatory dysfunctionY. L. Lai, and K.-R. Zhou1 January 1997 | Journal of Applied Physiology, Vol. 82, No. 1Axon reflex in resiniferatoxin-induced bronchoconstriction of guinea pigsRespiration Physiology, Vol. 92, No. 1Evoked bronchoconstriction: testing three methods for measuring respiratory mechanicsRespiration Physiology, Vol. 77, No. 1Fluid trapping in postmortem guinea pig lungsLung, Vol. 165, No. 1Lung Recoil: Elastic and Rheological Properties1 January 2011Mechanics of the Pleural Space1 January 2011Methods and Results of Postmortem Studies of Airway Dynamics in Normal Lungs and Lungs with Minimal ObstructionPHARMACOLOGICAL RESPONSES OF HUMAN AND PORCINE LUNG PARENCHYMA, BRONCHUS AND PULMONARY ARTERY19 July 2012 | British Journal of Pharmacology, Vol. 76, No. 4Methods of study of airway smooth muscle and its physiologyPharmacology & Therapeutics, Vol. 7, No. 2Maximal Midexpiratory Flow as an Index of Acute Airway ChangesChest, Vol. 68, No. 6Vertical gradients of pleural and transpulmonary pressure with liquid-filled lungsRespiration Physiology, Vol. 23, No. 2Effect of histamine on the vertical gradient of transpulmonary pressureRespiration Physiology, Vol. 20, No. 3 More from this issue > Volume 30Issue 5May 1971Pages 691-702 https://doi.org/10.1152/jappl.1971.30.5.691PubMed5572792History Published online 1 May 1971 Published in print 1 May 1971 Metrics