The physiologic responses to epinephrine during cooling and after rewarming in vivo

The purpose of our study was to determine whether hypothermia has any effects on physiological hemodynamic responses to epinephrine (Epi), and whether rewarming reverses these effects.

Sprague-Dawley rats were instrumented to measure mean arterial pressure (MAP), and left ventricular (LV) pressure-volume changes were recorded by using a Millar pressure-volume conductance catheter. Core temperature was reduced from 37°C to 28°C and returned to 37°C by using both internal and external heat exchangers. Two groups of rats were infused with either saline (n = 7), or Epi 0.125 μg/min continuously (n = 7). At 33°C, 30°C, and 28°C, the Epi infusion was temporarily increased from 0.125 to 1.25 μg/min.

Before cooling, Epi infusion in both groups resulted in a significant, dose-dependent increase in heart rate (HR), stroke volume (SV), cardiac output (CO), LV dP/dtmax (maximum derivative of systolic pressure over time), but only Epi infusion at 1.25 μg/min caused elevation of MAP. During cooling to 30°C, Epi infusion at 0.125 μg/min caused a significant elevation of central hemodynamic variables, whereas MAP remained unchanged. In contrast, Epi infusions at 1.25 μg/min caused a significant elevation of MAP during cooling to 28°C but no increases in central hemodynamics. After rewarming, all hemodynamic variables returned to baseline in both groups, but only the saline-treated animals displayed the prehypothermic hemodynamic dose responses to Epi infusions.

This study shows that hypothermia causes a change in the physiological hemodynamic response to Epi, which is not reversed by rewarming.