Abnormal pulmonary slowly adapting receptors in canine acrylamide neuropathy

Slowly adapting lung stretch receptors (SARs) and their vagal afferents are considered to play an important role in the mediation of numerous respiratory reflexes. The understanding of such reflexes has been facilitated by altering the discharge properties of SARs or by preventing the conduction of SAR-generated impulses to the brain stem. In a number of naturally occurring diseases of the peripheral nervous system, the vagus nerve and vagal reflexes are damaged. We have studied the function of SARs in anesthetized dogs with acrylamide neuropathy, a distal axonopathy that has been used as a model of naturally occurring neuropathies. There was a marked increase in threshold and decrease in firing rate of SARs in dogs with moderate neuropathy. Abnormal SAR discharge patterns were observed, and there was a depletion of those units innervated by the fastest conducting vagal afferent fibers in treated animals. Acrylamide induced degeneration of myelinated fibers in bronchial branches of the vagus nerve. These abnormalities were partially reversed upon withdrawal of the neurotoxin. Acrylamide may be a useful agent in the study of vagally mediated respiratory reflexes. SAR function is likely to be abnormal in diseases of the peripheral nervous system.