Although ethyl alcohol has a long medicinal history (1), its precise effects on the cardiovascular system have not been defined. Acute alcohol ingestion is known to result in triglyceride accumulation in the liver, which appears dependent upon an intact sympathetic nervous system (2). Evidence for stimulation of this system after ethanol ingestion has been advanced (3). Since sustained catecholamine infusion has been associated with lipid accumulation in the myocardium (4, 5), a study of the acute effects of ethanol on myocardial metabolism and function has been undertaken in animals considered nutritionally normal. The quantity given produced blood level concentrations usually associated with moderate intoxication. MethodsMongrel male dogs weighing 19 to 22 kg were anesthetized 18 hours postprandially with morphine sulfate, 3 mg per kg, and pentobarbital (Nembutal), 12 mg per kg, and studied without opening the chest. After insertion of an endotracheal tube, respiration was regulated with a Harvard respiratory pump, facilitating the maintenance of arterial oxygen saturation and pH in the normal range. Catheters were placed in the coronary sinus, pulmonary artery, aorta, and left ventricle for blood sampling and pressure determinations. Although initially the catheters were filled with dilute heparin, slow saline infusions or intermittent flushes were used during the experiment to maintain their patency. Since the level of arterial free fatty acids did not rise during the experiment, the earlier limited use of heparin did not appear to affect substrate concentrations.During the evaluation of cardiac performance in the intact animal in experiments of many hours duration, a direct measurement of contractility utilizing the forcevelocity relationship is not feasible, but less direct methods may be employed to characterize myocardial function. Thus, contractility change has been deduced from the relation of stroke output to left ventricular end-diastolic pressure (LVEDP) (6, 7).Sympathetic stimulation of isolated papillary muscle analyzed in terms of the force-velocity relationship has revealed an enhanced velocity of muscle shortening, representing a primary contractility increase (8). Sympathetic stimulation of the intact heart under conditions of controlled heart rate, before and after loading, has evoked an increase of stroke output as well as dp/dt maximum of left ventricular pressure as manifestations of primary contractility increments (9).A rise in LVEDP is normally associated with a corresponding stroke output increment (9), presumably a reflection of the rise in maximal isometric force without a velocity change that attends increased length of papillary muscle (8). The failure of stroke output to rise in this situation would appear to represent impaired muscle function (6,9,10) particularly when the duration of systole is prolonged or unchanged (6). In this present study the ventricular ejection rate was analyzed in terms of ventricular systolic duration and the maximal rate of rise of left ventricular pres...

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Abstract. To assess the relation of ventricular arrhythmias to myocardial Ki movement during ischemia, we placed an electrode catheter in the left anterior descending coronary artery for thrombus production in intact anesthetized dogs. 85Kr injections distal to the thrombus permitted serial coronary blood flow measurements. Animals of Group I with a moderate flow reduction exhibited no arrhythmia or myocardial egress of K+. In Group II, marked flow reduction was accompanied by an injury potential and loss of K+ from the ischemic site, before and during ventricular tachycardia.Therapeutic interventions were performed in animals having the same degree of ischemia as Group II. Systemic procaine amide in Group III interrupted the tachycardia and egress of K+, despite persistent ischemia. Group IV did not respond to intracoronary insulin with K+ uptake, as did normal dogs, and progressed to fibrillation. During the production of hyperglycemia in Group V, myocardial loss of Ki ceased with maintenance of sinus rhythm.Hemodynamic factors did not appear to have a major role in the genesis of the arrhythmia.Since intracoronary infusion of Ki in normal dogs similarly altered repolarization and produced fibrillation, it would appear that during ischemia egress of Ki before development of the arrhythmia indicates a major role of the ion in pathogenesis. This view is supported by the myocardial loss of K+ and arrhythmia induced in normal dogs by strophanthidin and by the fact that pharmacologic regulation of K+ loss is associated with correction of the arrhythmia, despite persistence of low blood flow.

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