UNIQUE CIRCULATORY RESPONSES TO EXOGENOUS CATECHOLAMINES AFTER BRAIN DEATH1

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Abstract
For better management of brain-dead donors, we developed a small animal model of brain death.We investigated how three catecholamines commonly used for the management of donors affected the cardiac function, hemodynamics, and tissue blood flow in the endocardium and renal cortex. Thirty-two rabbits were divided into four groups. Group C served as a control. In group D, dopamine 10 μg/kg/min was infused from 15 to 180 min after brain death. Norepinephrine in group N and epinephrine in group A were infused at 0.5 μg/kg/min. Heart rate, mean arterial pressure, left ventricular developed pressure, left ventricular end-diastolic pressure (LVEDP), LV dP/dt, −peak dP/dt, endocardial flow, renal cortical flow, and their percent changes until 180 min after brain death were compared. Acute induction of brain death caused sudden but transient hyperdynamic conditions, followed by profound circulatory collapse. Dopamine and norepinephrine increased heart rate, blood pressure, and endocardial flow at the expense of a reduction in renal cortical flow and had little effect on the other variables. Epinephrine significantly increased all these variables, with the exception of left ventricular end-diastolic pressure and −peak dP/dt, without a corresponding reduction in renal cortical flow. Dopamine and norepinephrine impaired renal perfusion and may reduce the viability of renal grafts before retrieval. Epinephrine improved circulatory collapse and pump dysfunction after brain death, while simultaneously maintaining renal perfusion. We conclude that epinephrine should be selected as the catecholamine of choice for the management of brain-dead donors.