EFFECT OF HEATING ON THE HEMODYNAMIC-RESPONSES TO VASOACTIVE AGENTS

During hyperthermia, vasoconstrictor tone in the viscera is lost despi te high levels of sympathetic neural outflow and plasma catecholamines , suggesting that vascular responsiveness to adrenergic receptor stimu lation is reduced. The purpose of this study was to determine whether adrenoceptor-mediated control of vascular resistance is altered at hig h body core temperatures. The hemodynamic responses to adrenoceptor ag onists were examined in chloralose-anesthetized rats heated to colonic temperatures (T-co) of 37, 39, and 41.5 degrees C. Elevating T-co to 39 degrees C did not alter the hemodynamic responses to any of these a gents. Further heating to 41.5 degrees C markedly attenuated the hemod ynamic responses to alpha- and beta-adrenoceptor agonists. Similarly, the regional and systemic hemodynamic responses to ANG II and endothel in were also reduced at 41.5 degrees C. In contrast, the hemodynamic r esponses to endothelium-dependent and -independent vasodilator agents were unchanged or slightly reduced at 41.5 degrees C. The blunted hemo dynamic responses observed at 41.5 degrees C indicate that vascular re activity to vasoconstrictor agents is reduced with hyperthermia and su ggest that this nonspecific change in vascular responsiveness may cont ribute the circulatory collapse associated with high body temperatures .