Effect of hyperthermia on the hemodynamic responses to α- and β-adrenoceptor agonists

The loss of visceral vasoconstriction which precedes the onset of circulatory collapse during severe hyperthermia may be due to a reduction in vascular responsiveness to catecholamines. This study examined whether a loss of adrenoceptor-mediated regulation of vascular resistance at high core body temperatures (TJ occurs prior to the fall in arterial blood pressure. The hemodynamic responses to norepinephrine (NE, 0.5-2.5 μg/kg), phenylephrine (PE, 0.5-8.0 μg/kg), epinephrine (EPI, 0.25-2.0 μg/kg), and isoproterenol (ISO, 0.125-1.0 μg/kg) were examined in chloraloseanesthetized rats (n = 18) under normothermic (Tc = 37°C) and mildly (T_c = 39°C) and moderately (T_c = 41.5°C) hyperthermic conditions. The hemodynamic effects of the α- and β-adrenoceptor agonists were not modified by elevating Tc to 39°C. Raising Tc to 41.5°C increased mean arterial blood pressure, heart rate, and mesentenc vascular resistance (+23.3±5.3%), and decreased hindlimb resistance (-41.6±1.7%). Renal resistance was unchanged with heating. The vasoconstrictor effects of NE, PE, and EPI in the mesentenc and renal beds were markedly reduced at a Tc of 41.5°C, as were the NE- and PE-mediated vasoconstrictor responses in the hindlimb. The ISO-induced vasodilator responses in all three vascular beds were also markedly suppressed at this T_c. In conclusion, the blunted hemodynamic responses observed at 41.5°C indicate that vascular responsiveness to α- and β-adrenoceptor agonists is reduced with hyperthermia and suggests that a loss of adrenoceptor function may precede the circulatory collapse associated with high core body temperatures.