Abstract
In urethane-anesthetized rabbits with the right aortic nerve (RAN) sectioned, we examined the reflex heart rate (HR) responses during brain ischemia for approximately 30 s, by applying the anodal block to the unsectioned left aortic nerve (LAN) and, subsequently, by denervating the LAN. The maximum decreases in HR occurred at around 30 s after the onset of brain ischemia. The anodal block used in this study selectively inhibited the aortic A-fiber conduction but did not inhibit the volley of aortic C-fibers. The maximum HR fall responses to brain ischemia with and without the anodal block were 143 ± 7 and 183 ± 7 beats/min, respectively. When the maximum value of HR fall during brain ischemia in the absence of aortic nerve signals was subtracted from these two values, the reflex HR fall responses to brain ischemia with aortic C and A baroreceptor activation were 98 ± 7 and 43 ± 8 beats/min, respectively. In another series of experiments used for the same techniques, the reflex fall in HR seen during brain ischemia with the anodal block was totally abolished by vagotomy. The results indicate that the ability of aortic C baroreceptors becomes more prominent on the magnitude of brain ischemia-induced reflex bradycardia as compared to that of aortic A baroreceptors.
Published Version
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