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Airway smooth muscle (ASM) plays a vital role in the exaggerated airway narrowing seen in asthma. However, whether asthmatic ASM is mechanically different from nonasthmatic ASM is unclear. Much of our current understanding about ASM mechanics comes from measurements made in other species. Limited data on human ASM mechanics prevents proper comparisons between healthy and asthmatic tissues, as well as human and animal tissues. In the current study, we sought to define the mechanical properties of healthy human ASM using tissue from intact lungs and compare these properties to measurements in other species. The mechanical properties measured included: maximal stress generation, force-length properties, the ability of the muscle to undergo length adaptation, the ability of the muscle to recover from an oscillatory strain, shortening velocity and maximal shortening. The ultrastructure of the cells was also examined. Healthy human ASM was found to be mechanically and ultrastructurally similar to that of other species. It is capable of undergoing length adaptation and responds to mechanical perturbation like ASM from other species. Force generation, shortening capacity and velocity were all similar to other mammalian ASM. These results suggest that human ASM shares similar contractile mechanisms with other animal species and provides an important dataset for comparisons with animal models of disease and asthmatic ASM.

Human airway smooth muscle is structurally and mechanically similar to that of other species