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Postjunctional factors

Prejunctional and postjunctional factors in airway control

Neurogenic stimulation, cytokine and mediator release affect the system postjunctionally, as in the lower panel. These postjunctional factors potentially increase maximal airway narrowing. Smooth muscle hypertrophy and/or hyperplasia ( i ) leads to an enhanced contractile response. There is some evidence that in addition the inflammatory process in asthma is associated with increased actomyosin ATP-ase activity, leading to greater shortening velocity and greater maximal shortening.

Mediators and cytokines may be delivered to the airways via the circulatory system ( j ); they may be generated by processes outside the lung, or be locally produced and be transported down the airways by the bronchial circulation.

Adventitial swelling ( k ) increases the outer airway circumference, due to which smooth muscle contraction may be less opposed by the elastic pull from alveolar attachments. Increased airway secretions ( n ) and exudate diminish airway lumen and, together with increased airway compliance ( o ) amplify the effect of smooth muscle contraction. This may also be due to collagen deposition in the subepithelial reticular layer ( l ) associated with chronic inflammation in asthma, but then collagen might stiffen the airway. The submucosal swelling leads to diminished epithelial folding ( m ) and liquid filling of interstices between epithelial projections. The force developed by smooth muscle depends on its initial length (length-tension relationship); this is influenced by lung elastic recoil and hence lung volume ( p ), and loss of alveolar attachments ( q ). The latter factors also determine the elastic load to contracting muscles.

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