Abstract
Our purpose was to determine both if hypothermia has any effects on physiological hemodynamic response to isoproterenol (Iso) and if rewarming reverses these effects. Rats were instrumented to measure mean arterial pressure (MAP) and left ventricular (LV) pressure-volume changes using a Millar pressure-volume conductance catheter. Core temperature was manipulated from 37 °C (normothermia) to 24°C (hypothermia) and back to 37°C (rewarming) using both internal and external heat exchangers. During cooling at each temperature (33, 30, 27 and 24°C), central hemodynamic variables and MAP were measured while infusing Iso with the dose of 0.0017, 0.005, 0.01, and 0.02 μg · min-1, respectively. Seven animals underwent all phases of the protocol. At normothermia Iso infusion resulted in a significant, dose-dependent increase in heart rate (HR), stroke volume (SV), cardiac output (CO), LV dP/dtmax but no change in MAP. During cooling Iso infusion caused no significant change in any of the hemodynamic variables. After rewarming basal HR was increased, whereas SV and LV dP/dtmax were both significantly reduced when compared to their prehypothermic basal values, and they were non-responsive to Iso infusion. This study shows that hypothermia caused a change in physiological response to Iso, which was not reversed by rewarming.
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