Abstract
In anesthetized, paralyzed and ventilated rats, hypoxia, produced by intratracheal administration of 100% N 2 for 20 s, increases sympathetic nerve activity and produces cardiovascular responses. Acute midcollicular decerebration has no effect on these responses in chemo-innervated or chemo-denervated animals. Suprapontine neural structures are, therefore, not required for the rapid sympathetic and cardiovascular responses to acute hypoxia. The results support the view that sympathoexcitatory responses to acute hypoxia depend entirely on the functions of reticulospinal sympathoexcitatory vasomotor neurons of the rostral ventrolateral medulla (RVL).
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