Catecholamine-depletion and the no-reflow phenomenon in anoxic and ischaemic rat hearts

Abstract

The effect of depleting catecholamines in myocardium on the extent of the no-reflow phenomenon was investigated in isolated Langendorff rat heart preparations. Catecholamines were depleted by pretreating the rats with reserpine. After ischaemia or anoxia the proportion of the ventricular walls perfused by 1% fluorescein was assessed, and compared with the changes in glycogen content, lactate production, ATP levels and general morphology. After 60 min of global ischaemia, 60% of the ventricular walls of both catecholamine-depleted and untreated hearts was not reperfused. A similar period of anoxia produced 30% no-reflow in untreated controls, but only 16% in catecholamine-depleted hearts. Reserpine pretreatment caused a doubling of glycolytically derived ATP in anoxic hearts. However, in catecholamine-depleted ischaemic hearts there was no increase in ATP because of an inhibition of glycolysis, presumably due to the fall in pH. These findings indicate that, in anoxia, catecholamine depletion delays the onset of no-reflow by prolonging anaerobic ATP generation due to increased glycogen stores, and in global ischaemia at least, the no-reflow phenomenon is not due to catecholamine-induced sustained contraction of coronary arteries.