[Brain death: myocardial consequences, an experimental study on pigs]

It is well known that brain death is responsible for major problems encountered in the clinical setting that may alter heart graft viability before transplantation. To investigate these myocardial dysfunctions, a model of brain death was prepared in pigs. Anaesthetised pigs were ventilated with FiO2 of 50% through an endotracheal tube. Animals were monitored by measuring systemic arterial pressure, pulmonary artery pressure, cardiac output, left ventricular developed pressure and dP/dT (Millar probe), cardiac contractility (sonomicrometers crystals), ECG, myocardial tissue oedema (impedance spectroscopy) and heart rate. Blood samples were drawn to assess arterial blood gases, serum electrolytes, plasma catecholamine levels, LDH isoenzymes and ascorbil free radicals production. Myocardial high energy contents (adenosine triphosphate, creatine phosphate) were measured by spectroscopy MRI. After 30 minutes stabilisation, brain death was induced by ligation of the supra-aortic vessels. To assess myocardial impairment all the parameters mentioned were recorded at baseline, 1', 30', 60', 120' and 180' following the brain death. Results showed initial tachycardia and a significant increase (p < 0.05) in cardiac function at 1' and 30', related to the cathecolamine level variations, followed by a significant depression (p < 0.05) of cardiac contractility by the end of the third hour; there was no modification whatsoever of myocardial high energy contents and of ascorbil free radical and LDH isoenzymes productions. In this pig model of brain death the observed myocardial dysfunction was directly related to the induced catecholamine secretion without any myocardial high energy substrate depletion up until 180'. Such results could be taken into account when evaluating a donor heart, allowing to use organs judged nowadays not feasible, and could be of some help in lowering the number of the "défaillances" of the transplanted hearts.