1. The isolated perfused non-working rat heart, subjected to low coronary flow, has been used to study the effects of myocardial ischaemia on both the mechanical and metabolic performance of the heart.

2. In this preparation, adrenaline initially increased developed tension and heart rate, followed shortly thereafter by marked deterioration in mechanical performance to levels below those observed in the control state. These latter responses occurred simultaneously with stimulation of endogenous myocardial lipolysis. The rate of release of non-esterified fatty acids was positively correlated with both the decline in developed tension and the rise in resting tension.

3. The anti-lipolytic agent nicotinic acid had no effect on the initial mechanical responses of the heart to adrenaline but prolonged the period of enhanced tension development after adrenaline and reduced the degree of later deterioration in performance, in addition to blocking lipolytic stimulation.

4. Hearts from rats fed on a diet rich in animal fat contained larger triglyceride reserves and exhibited greater rates of non-catecholamine-stimulated lipolysis than hearts from normally fed rats. During ischaemic perfusion such hearts showed a more marked rise in resting tension and decline in heart rate than hearts from normally fed animals. Such hearts also had an increased incidence of arrhythmias and a slight reduction in developed tension. The initial responses of these hearts from fat-fed rats to adrenaline were also depressed as compared with normal hearts. Hearts from fat-fed rats showed a greater tendency to deteriorate in performance after adrenaline, particularly with falling heart rates and the onset of ventricular fibrillation.

5. We suggest that these results indicate that myocardial lipolysis makes a significant contribution to the adrenaline-induced deterioration in performance seen in these ischaemically perfused rat hearts.

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