Myocardial contractility in a canine model of the brain-dead organ donor

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Abstract

Objective:

To test the hypothesis that the induction and maintenance of brain death leads to a decease in myocardial contractility.

Design:

Prospective, randomized, controlled trial.

Setting:

Laboratory at a large, university affiliated medical center.

Subjects:

Sixteen adult, male, mongrel dogs weighing 15 to 25 kg.

Interventions:

Myocardial contractile performance was evaluated after the induction of either brain death (n = 8), sham brain death (n = 4), or an operative procedure serving as a time control (n = 4). Brain death was induced by increasing and maintaining intracranial pressure above arterial systolic pressure. Contractile performance was determined with sonomierometers arrayed to measure wall thickness in the anterior and posterolateral left ventricle. Brief aortic constrictions enabled derivation of the end-systolic pressure-thickness relationship, a relatively load-insensitive index of contractility.

Measurements and Main Results:

No statistically significant hemodynamic differences were detected between the sham and time control groups. The brain-dead group displayed marked hemodynamic deterioration; 4 hrs after brain death was induced, mean arterial blood pressure, cardiac index, and the peak positive first derivative of left ventricular pressure were 63%, 35%, and 53% lower, respectively, than those values in the two control groups. However, the slope of the end systolic pressure-thickness relationship remained at 92 ± 12% of baseline levels 4 hrs after brain death was induced and was not significantly different from the two control groups.

Conclusions:

The hemodynamic deterioration after the induction of brain death could not be attributed to a decrease of myocardial contractility as measured by the end systolic pressure-thickness relationship. (Crit Care Med 1993; 21:1731–1739)

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