Abstract
In rats anesthetized with urethane, electrical stimuli applied to tibial nerve afferents produced a somato-sympathetic A-reflex of 41 ± 2 (mean ± SEM) ms latency and C-reflex of 210 ± 13 ms latency recorded in the left inferior cardiac sympathetic nerve. Hypoxia was induced by switching room air to nitrogen/oxygen gas mixture in the inspiratory line reducing end-tidal oxygen from about 18% F ET o 2 to 10% F ET o 2 and 6% F ET o 2 for 60 s, respectively. During 6% F ET o 2 hypoxia, the amplitude of the somato-cardiac sympathetic A-reflex increased significantly to 138 ± 13% of the control, and that of the C-reflex increased to 186 ± 18% of the control. During 10% F ET o 2 hypoxia, the A-reflex increased insignificantly to 117 ± 8%; the amplitude of the C-reflex was augmented significantly to 149 ± 11% of the control. Peripheral carotid chemoreceptor denervation abolished the facilitatory effects of systemic hypoxia. It is concluded that carotid chemoreceptor stimulation enhances the responsiveness of somato-cardiac sympathetic excitatory reflexes originating in the hind limb receptors.
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