Effect of heating on the hemodynamic responses to vasoactive agents

During hyperthermia, vasoconstrictor tone in the viscera is lost despite high levels of sympathetic neural outflow and plasma catecholamines, suggesting that vascular responsiveness to adrenergic receptor stimulation is reduced. The purpose of this study was to determine whether adrenoceptor-mediated control of vascular resistance is altered at high body core temperatures. The hemodynamic responses to adrenoceptor agonists 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 agents. Further heating to 41.5 degrees C markedly attenuated the hemodynamic responses to alpha- and beta-adrenoceptor agonists. Similarly, the regional and systemic hemodynamic responses to ANG II and endothelin were also reduced at 41.5 degrees C. In contrast, the hemodynamic responses to endothelium-dependent and -independent vasodilator agents were unchanged or slightly reduced at 41.5 degrees C. The blunted hemodynamic responses observed at 41.5 degrees C indicate that vascular reactivity to vasoconstrictor agents is reduced with hyperthermia and suggest that this nonspecific change in vascular responsiveness may contribute the circulatory collapse associated with high body temperatures.