Mechanical Properties of Sensitized Airway Smooth Muscle: Shortening Capacity

Abstract

Fig. 1. Schematic drawing of Voigt's model. SEC::: series elastic component; CE ::: contractile element; PEC ::: parallel elastic component. Importance of Maximal Shortening Capacity of Airway Smooth Muscle Because of the nonspecificity of the increased contractile response of antigen-sensitized airway smooth muscle (SASM), the idea has developed that the primary cause of allergic bronchospasm resides in the contractile apparatus of the SASM (1). In 1979 we studied this possibility and reported (2) that in the ovalbumin-sensitized SASM, both the capacity to shorten (~lmax) and the maximal velocity of shortening (V0) were significantly greater than in the control airway smooth muscle. Interestingly, maximal isometric tetanic tension (Po) remained normal in the SASMs that had been obtained from 2-month-old pups. We concluded that Po is a poor and tardy index of altered contractility. The important finding emerging from this study was the increased ~lmax because it represented the important in vitro analogue to in vivo bronchospasm. It indicated that elucidation of bronchospasm must necessarily focus on mechanisms controlling extent of shortening. Although V0 also increased, suggesting that changes had occurred in the myosin molecule and its enzymatic properties, these did not relate directly to allergic bronchospasm. Recently, we conducted studies (3) on tracheal smooth muscle (TSM) from rats with congenitally hyperreactive airways and obtained similar results. We now describe the results of studies we have reported in the past (4) that deal with