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This study tested the hypothesis that passive heating impairs cerebral autoregulation. Transfer function analyses of resting arterial blood pressure and middle cerebral artery blood velocity (MCA V(mean)), as well as MCA V(mean) and blood pressure responses to rapid deflation of previously inflated thigh cuffs, were examined in nine healthy subjects under normothermic and passive heat stress (increase core temperature 1.1 +/- 0.2 degrees C, P 0.5 and similar between normothermia and heat stress in the low- (0.07-0.20 Hz, P = 0.40) and high-frequency (0.20-0.35 Hz, P = 0.12) ranges. Transfer gain was reduced during heat stress in the very-low-frequency (0.88 +/- 0.38 to 0.59 +/- 0.19 cm.s(-1).mmHg(-1), P = 0.02) range, but was unaffected in the low- and high-frequency ranges. The magnitude of the decrease in blood pressure (normothermia: 20 +/- 4 mmHg, heat stress: 19 +/- 6 mmHg, P = 0.88) and MCA V(mean) (13 +/- 4 to 12 +/- 6 cm/s, P = 0.59) in response to cuff deflation was not affected by the thermal condition. Similarly, the rate of regulation of cerebrovascular conductance (CBVC) after cuff release (0.44 +/- 0.22 to 0.38 +/- 0.13 DeltaCBVC units/s, P = 0.16) and the time for MCA V(mean) to recover to precuff deflation baseline (10.0 +/- 7.9 to 8.7 +/- 4.9 s, P = 0.77) were not affected by heat stress. Counter to the proposed hypothesis, similar rate of regulation responses suggests that heat stress does not impair the ability to control cerebral perfusion after a rapid reduction in perfusion pressure, while reduced transfer function gain and coherence in the very-low-frequency range during heat stress suggest that dynamic cerebral autoregulation is improved during spontaneous oscillations in blood pressure within this frequency range.
Low et al. (Thu,) studied this question.