Abstract
To determine if denervation of the carotid sinus region to eliminate arterial chemoreceptor inputs alters the mean arterial pressure (MAP) response to exposures to IH, the carotid sinus nerves were sectioned bilaterally in rats and the carotid bifurcation region painted with phenol. After a one week recovery period, rats were instrumented with telemetry transmitters. After a one week recovery period, the denervation was considered adequate if a 10 min reduction in inspired O2 to 10% resulted in a fall in MAP instead of the increase in MAP observed in carotid sinus nerve intact rats. Carotid denervated rats (n=7) and carotid intact rats (13) were exposed to IH (7 days for 8 hr/day, 3 min room air alternating with 3 min 10% O2). During the period of the day when exposed to IH, there was a significant effect of IH on MAP (p=.003). In intact rats MAP on control days was significantly different from the IH exposure days (p=.001) but not in denervated rats (p=.067). During the dark period of the day there was a significant effect of IH on MAP (p=.001) but no difference between intact and denervated rats. The change in MAP during the control period (average of control days 3–7) compared to during IH exposure (average of days 3–7) was 6.1±0.5mmHg in intact rats and −2.29±0.7mmHg in denervated rats during the period of the day when exposed to IH (p ≤ .001) and 5.9±0.2mmHg in intact rats and 4.2±0.6mmHg in denervated rats during the dark period of the day (p=.028). In conclusion, the arterial chemoreceptors prevent falls in MAP during exposure to IH, and mechanisms independent of the arterial chemoreceptors are capable of increasing MAP following exposure to IH.
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