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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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