ArticleAmerican journal of physiology. Lung cellular and molecular physiology2011
Could an increase in airway smooth muscle shortening velocity cause airway hyperresponsiveness?
Article in American journal of physiology. Lung cellular and molecular physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
14 citing papers in PubMed, 29 citations in OpenAlex.
- Airway smooth muscle function in asthma.Frontiers in physiology · 2022Review
- Peripheral Airway Smooth Muscle, but Not the Trachealis, Is Hypercontractile in an Equine Model of Asthma.American journal of respiratory cell and molecular biology · 2016Article
- Airway Hyperresponsiveness to Mannitol in Obesity Before and After Bariatric Surgery.Obesity surgery · 2015Observational
- Human trachealis and main bronchi smooth muscle are normoresponsive in asthma.American journal of respiratory and critical care medicine · 2015Article
- Mechanisms of airway hyper-responsiveness in asthma: the past, present and yet to come.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2015Review
- Modeling the impairment of airway smooth muscle force by stretch.Journal of applied physiology (Bethesda, Md. : 1985) · 2015Article
- Phenotype, endotype and patient-specific computational modelling for optimal treatment design in asthma.Drug discovery today. Disease models · 2015Article
- CD4+ T cells enhance the unloaded shortening velocity of airway smooth muscle by altering the contractile protein expression.The Journal of physiology · 2014Article
- Dissociation of FK506-binding protein 12.6 kD from ryanodine receptor in bronchial smooth muscle cells in airway hyperresponsiveness in asthma.American journal of respiratory cell and molecular biology · 2014Article
- Mechanical correlates of dyspnea in bronchial asthma.Physiological reports · 2013Article
- Counterpoint: alterations in airway smooth muscle phenotype do not cause airway hyperresponsiveness in asthma.Journal of applied physiology (Bethesda, Md. : 1985) · 2012Article
- A multi-scale approach to airway hyperresponsiveness: from molecule to organ.Frontiers in physiology · 2012Article
- Accumulating evidence for increased velocity of airway smooth muscle shortening in asthmatic airway hyperresponsiveness.Journal of allergy · 2012Article
- Myosin filament polymerization and depolymerization in a model of partial length adaptation in airway smooth muscle.Journal of applied physiology (Bethesda, Md. : 1985) · 2011Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 3 countries.
Funding
Abstract
Airway hyperresponsiveness (AHR) is a characteristic feature of asthma. It has been proposed that an increase in the shortening velocity of airway smooth muscle (ASM) could contribute to AHR. To address this possibility, we tested whether an increase in the isotonic shortening velocity of ASM is associated with an increase in the rate and total amount of shortening when ASM is subjected to an oscillating load, as occurs during breathing. Experiments were performed in vitro using 27 rat tracheal ASM strips supramaximally stimulated with methacholine. Isotonic velocity at 20% isometric force (Fiso) was measured, and then the load on the muscle was varied sinusoidally (0.33 ± 0.25 Fiso, 1.2 Hz) for 20 min, while muscle length was measured. A large amplitude oscillation was applied every 4 min to simulate a deep breath. We found that: 1) ASM strips with a higher isotonic velocity shortened more quickly during the force oscillations, both initially (P < 0.001) and after the simulated deep breaths (P = 0.002); 2) ASM strips with a higher isotonic velocity exhibited a greater total shortening during the force oscillation protocol (P < 0.005); and 3) the effect of an increase in isotonic velocity was at least comparable in magnitude to the effect of a proportional increase in ASM force-generating capacity. A cross-bridge model showed that an increase in the total amount of shortening with increased isotonic velocity could be explained by a change in either the cycling rate of phosphorylated cross bridges or the rate of myosin light chain phosphorylation. We conclude that, if asthma involves an increase in ASM velocity, this could be an important factor in the associated AHR.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.