Active expiration and sympathetic overactivity induced by short‐term sustained hypoxia in rats

Abstract

Short‐term sustained hypoxia (SH, 24 hrs) produces changes in the respiratory motor activity. However, the neurochemical and electrophysiological basis of these changes are poorly understood. In the present study, we evaluated the central mechanisms underlying the respiratory changes induced by SH (10% O2) and the correlated changes in sympathetic activity. Using arterially‐perfused in situ preparations, we observed that SH rats (n=20), but not controls, exhibited late‐expiratory (late‐E) bursts in abdominal nerve (P<0.05) associated with depressed post‐inspiratory and increased augmenting‐expiratory activities of neurons in the Bötzinger complex (BötC, P<0.05). SH rats also exhibited additional late‐E bursts in thoracic sympathetic activity associated with larger Traube‐Hering wave amplitudes (P<0.05). Corroborating these findings, we observed in unanesthetized rats that the arterial pressure levels of SH rats (n=7) exhibited augmented low‐and high‐frequency variabilities (P<0.05). Besides, the antagonism of ionotropic glutamate receptors in the BötC eliminated the late‐E activity in respiratory and sympathetic nerves. Our data indicate that short‐term SH alters the expiratory pattern and its coupling with sympathetic nervous system by mechanisms involving changes of neuronal activities and glutamatergic transmission in the BötC.