Individuals experiencing high altitudes frequently exhibited respiratory and autonomic adjustments as a consequence of the exposure to sustained hypoxia (SH). However, the responses to SH may be inappropriate and cause serious ventilatory and circulatory maladaptations. We have been exploring the central mechanisms underlying the cardiorespiratory adjustments to SH. Using the decerebrated arterially-perfused in situ preparations of rats, we verified that SH exposure (10% O2 for 24 h) transforms the expiratory pattern into an active process, with the emergence of additional bursts in the abdominal motor activity during late-expiration (late-E). Coupled with augmented expiratory activity, additional late-E bursts in the thoracic sympathetic nerve as well as larger Traube-Hering pressure waves were observed in SH rats. In agreement with these in situ findings, rats submitted to SH exhibited elevated baseline arterial pressure associated with augmented low- and high-frequency variabilities in conscious state. The firing frequency of RVLM pre-sympathetic (n = 11) and BötC augmenting-expiratory (n = 10) neurons during late-E period were significantly higher in SH rats; however no changes were observed in their intrinsic electrophysiological properties. On the other hand, we observed that SH activated the late-E neurons of the retrotrapezoid nucleus (RTN), which may provide a necessary excitatory drive to generate abdominal and sympathetic late-E activities in SH rats. Altogether, the data indicate that SH for 24 hours alters the central generation the expiratory activity and its coupling with sympathetic activity by mechanisms involving changes RTN late-E neuronal activity. Financial Support: FAPESP and CNPq.
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Received: May 15, 2013
© 2013 Published by Elsevier Inc.