Key result
Human bronchial smooth muscle from patients with asthma exhibits significantly greater maximum capacity and velocity of shortening compared to healthy siblings.
Cultured airway smooth muscle cells that alter their phenotype to become highly contractile may serve as excellent models for studying the increased contractility seen in asthmatic airway smooth muscle.
Early airway smooth muscle shortening may affect bronchospasm timing assessments; leaves open velocity's determining role in vivo.
Qualitatively the mechanical, structural, and biochemical properties of airway smooth muscles resemble those of all other smooth muscle. However, one important distinguishing feature of airway smooth muscle is that the major portion of isotonic shortening is completed within the first 3 s in a muscle whose contraction is 10 s. This indicates the importance of focusing on the changes that occur in these 3 s and also the limiting role of the maximum velocity of shortening in determining shortening data. There is evidence that the maximum capacity and velocity of shortening in human bronchial smooth muscle from patients with asthma are significantly greater than those obtained from healthy siblings. In the demonstration in which cells in culture are arrested by withdrawing all fetal calf serum, the cells alter their phenotype to cells that are very long (more than 200 micrometers) and shorten twice as much as cells freshly isolated when the tissue is new. Speculatively, if such cells developed in vivo they could account for the increased contractility of asthmatic airway smooth muscle. These cultured cells could also be excellent models for study of airway smooth muscle contractility.
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Stephens et al. (1998) conducted a review in Asthma. Human bronchial smooth muscle from patients with asthma exhibits significantly greater maximum capacity and velocity of shortening compared to healthy siblings.
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