BRIEF PERFUSION WITH DILUTED WHOLE-BLOOD AFTER GLOBAL MYOCARDIAL-ISCHEMIA INCREASES REPERFUSION INJURY

Objectives: In vivo studies indicate that blood components, especially leucocytes, contribute to reperfusion injury after myocardial ischaem ia. This study was designed to: (1) develop a small animal heart model of ischaemia-reperfusion that demonstrates the contribution of blood to reperfusion injury; (2) determine when the presence of blood in the heart - that is, during ischaemia or during early reperfusion - cause d greater dysfunction; and (3) attempt to limit the blood contribution to reperfusion injury by leucocyte depletion. Methods: Adult rat hear ts were perfused in situ with a Krebs-albumin red cell solution (K2RBC ), then isolated. Cardiac pump function was assessed with an intravent ricular balloon as left ventricular developed pressure and contractili ty (dP/dt). Group I served as a non-ischaemic control group. Group II was subjected to global, no flow ischaemia for 30 min followed by 45 m in reperfusion. In group III, diluted whole blood replaced the K2RBC f or five min immediately before ischaemia. In group IV, diluted whole b lood was perfused during the first five min reperfusion. In group V, t he hearts were reperfused With leucocyte poor diluted whole blood. Res ults: Pre-ischaemic pump function values were similar to other blood p erfused, isolated heart models. Group I showed no increase in coronary resistance or decrease in pump function with time or in response to d iluted whole blood. After 35 min reperfusion, the recovery (% control) of dP/dt in group II was 56(12), in group III it was 39(15) and in gr oup IV it was only 19(6) (p < 0.05). Large increases in coronary vascu lar resistance, oedema, and contracture during reperfusion were also s een in group IV. When leucocytes were depleted from the diluted whole blood (group V), the recoveries were similar to reperfusion without di luted whole blood (group II). Conclusions: Thirty min of global, normo thermic ischaemia caused significant cardiac dysfunction early during reperfusion. Perfusion with unstimulated blood for a limited period fu rther impaired the recovery of function and enhanced myocardial oedema . Dysfunction was particularly evident when diluted whole blood was pe rfused during the first minutes of reperfusion. The leucocyte depletio n studies suggest that leucocytes are necessary, but may not be suffic ient, to demonstrate the blood contribution to reperfusion injury.