Why the study?
Does intravenous verapamil reduce vulnerability to ventricular fibrillation during myocardial ischaemia and reperfusion in a canine model?
Does intravenous verapamil reduce vulnerability to ventricular fibrillation during myocardial ischaemia and reperfusion in a canine model?
In a canine model, verapamil protects against ventricular fibrillation during myocardial ischemia and reperfusion, likely by antagonizing enhanced adrenergic input.
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Supports verapamil's anti-VF effects in canine ischemia-reperfusion; hypothesis-generating, with clinical translation remaining open.
The effects of verapamil on vulnerability to ventricular fibrillation were studied in 55 chloralose-anaesthetised dogs. Ventricular fibrillation threshold was measured before and during a 10 min period of left anterior descending coronary artery occlusion and following abrupt release of occlusion. The action of intravenous verapamil (0.01 mg.kg-1.min-1, following a 0.1 mg.kg-1 bolus) on vulnerability to fibrillation was examined before and during coronary artery occlusion and reperfusion. While the infusion of verapamil did not alter the ventricular fibrillation threshold in the nonischaemic myocardium, the vulnerable period threshold was raised and the incidence of spontaneous ventricular fibrillation was reduced both after coronary artery occlusion and release. Since cardiocardiac sympathetic reflexes are elicited in response to coronary artery occlusion, the effect of verapamil on vulnerability during left stellate ganglion stimulation and during noradrenaline infusion was investigated. Verapamil completely prevented the reduction in vulnerable period threshold during sympathetic nerve stimulation or noradrenaline infusion. This study suggests that the antifibrillatory action of verapamil during coronary artery occlusion may be, in part, related to antagonism of enhanced adrenergic input to the heart, while the mechanism of protection during reperfusion is as yet uncertain.
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Brooks et al. (1980) studied this question.
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