THE EFFECT OF BRAIN-DEATH ON CARDIOVASCULAR FUNCTION IN RATS - PART I- IS THE HEART DAMAGED

Objective: Brain death induces important haemodynamic changes in rats, with a drop in arterial blood pressure, left ventricular developed pr essure and dP/dt(max) to less than 50% of its control value. Myocardia l damage was reported to contribute to this paradigm. The role of pote ntial underlying pathogenetic mechanisms, such as a circulating cardio depressant factor, NO, endogenous opioid peptides, vagal or beta-adren ergic activation, or hypophyseal dysfunction, were explored, but none of them could be demonstrated as the culprit. This study investigated whether functionally important intrinsic myocardial damage was induced by brain death in the rat, and whether coronary endothelial cell dysf unction, possibly causing multifocal ischaemia, contributed to this. M ethods: Brain death was induced in rats by sudden inflation of an intr acranial balloon. Extensive haemodynamic measurements, including heart rate, arterial blood pressure, central venous pressure, left ventricu lar pressure, and cardiac output, were performed. Hearts excised 1 and 4 h after brain death were examined histologically. The contractile r eserve of these hearts was tested by administration of increasing dose s of adrenaline (10(-9) to 10(-6) mol/l) in a Langendorff system. The coronary endothelium was tested with regard to its barrier function fo r macromolecules by determining the extravasation of injected Evens bl ue, and with regard to its vasoactive function by testing the effects of serotonin and nitroglycerin in a Langendorff system. Results: The h aemodynamic measurements suggested that the cardiovascular collapse co nsisted mainly in alterations in afterload. Contractile reserve, as te sted with increasing adrenaline doses, revealed a normal dose-response curve. No histological myocardial damage was found after brain death in rats. No abnormal extravasation of Evans blue was seen. Coronary va soreactivity towards nitroglycerin and serotonin was normal. Conclusio n: Myocardial damage, if present at all, contributes only minimally to the changes in haemodynamic profile seen after brain death in the rat , and the coronary endothelium appears to preserve its barrier and vas oactive function. (C) 1998 Elsevier Science B.V.