THE EFFECTS OF DISOPYRAMIDE PHOSPHATE ON EARLY POST‐CORONARY ARTERY LIGATION DYSRHYTHMIAS AND ON EPICARDIAL ST‐SEGMENT ELEVATION IN ANAESTHETIZED DOGS

Open Access
Publisher Website
Google Scholar
Abstract
The antidysrhythmic, haemodynamic and metabolic effects of intravenously administered disopyramide phosphate (1 to 5 mg/kg) have been studied in greyhounds, anaesthetized with trichloroethylene. In doses of 2.5 and 5.0 mg/kg, disopyramide significantly reduced the ventricular dysrhythmias that occur in the initial 30‐min period following acute coronary artery ligation. None of the disopyramide‐treated animals developed ventricular fibrillation. The metabolic consequences of coronary artery ligation, assessed by local coronary venous sampling from the ischaemic area, were not modified by disopyramide except that K+ egress was prevented. There was evidence for substantial disopyramide‐induced myocardial depression (decreased cardiac output and left ventricular dP/dtmax with elevated ventricular filling pressure and pulmonary oedema and shunting) and it is suggested that great care be taken when the drug is administered intravenously in conditions where cardiac function is already compromised. Disopyramide also reduced myocardial blood flow. In chloralose‐anaesthetized mongrel dogs, disopyramide (2.5 mg/kg) significantly reduced the ST‐segment elevation (assessed from epicardial recordings) that resulted from short (3 min) coronary artery occlusions. This could indicate a reduction in the extent and severity of myocardial injury or simply reflect decreased K+ efflux (since locally administered K+ itself increased ST‐segment elevation).