ARTERIAL BAROREFLEX MODULATION OF HEAT-INDUCED VASODILATION IN THE RABBIT EAR

The purpose of this study was to determine whether nonthermal barorefl exes arising from cardiopulmonary and/or arterial baroreceptors modula te rabbit ear blood flow (EBF) during hyperthermia. Intact and sinoaor tic-denervated (SAD) rabbits were chronically instrumented with a Dopp ler ultrasonic flow probe for measurement of EBF velocity (kHz). Durin g whole body heating in conscious rabbits, EBF and ear vascular conduc tance (EVC) increased as core temperature increased until maximal plat eau levels of EBF and EVC were reached. The maximal plateau level of E VC attained during heat stress was lower in SAD than in intact rabbits . Subsequent intrapericardial administration of procaine at maximal EB F blocked cardiac afferents but did not alter EVC in either animal gro up. In a second experiment, ramp decreases in mean arterial pressure w ere produced by vena caval occlusion at maximal EBF. In intact rabbits , EBF and EVC decreased linearly as mean arterial pressure fell, but E BF and EVC did not decrease during vena caval occlusion in SAD rabbits . Thus neither pharmacological nor mechanical unloading of cardiac bar oreceptors results in reflex vasoconstriction in the heat-stressed rab bit ear. However, baroreflexes arising from arterial baroreceptors may modulate EBF in heat-stressed rabbits.