Smooth muscle shortening is determined by the force the muscle can develop in response to a stimulus, and by the forces that antagonize smooth muscle shortening (afterload). In intrapulmonary airways, a decrease in airway diameter due to muscle contraction is opposed by the surrounding lung parenchyma. This tethering effect of the lung parenchyma on the airway is an elastic afterload opposing muscle shortening. The lung parenchyma and smooth muscle interact to affect smooth muscle shortening and airway narrowing. The elastic load from the lung parenchyma increases with increasing lung volume. Maximal airway narrowing during bronchoconstriction is greater at low lung volumes, when the elastic load is lower than at high lung volumes.
The animation (to the right) illustrates how airway narrowing due to smooth muscle contraction is affected by the tethering forces of the lung parenchyma.
Click on picture for an interactive presentation of the measurement of lung recoil, and the relationship between lung elastic recoil and lung volume.
Elastic recoil pressure increases with lung volume; the outer surface area of the airways is similarly volume dependent. The alveoli attach to the outer airway wall. The pressure exerted via alveolar attachments at the airway surface is elastic force (Fel) divided by surface area (A). If the ratio increases, so does the pressure that needs to be overcome by contracting muscles. The initial length of the smooth muscle, influenced by lung volume, will determine whether the smooth muscle contracts near its optimal length to generate maximal force. Also consider what happens if edema produces swelling of the outer surface of the airway. In that case A increases, Fel is not necessarily affected, the number of attachments is the same, and the elastic afterload decreases. We shall skip the influence of surface active forces as the airway dimensions change or when the properties of fluid lining the epithelial cells change.
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