The effect of verapamil on reperfusion arrhythmia in canine heart.

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Abstract
This study was designed to clarify the mechanism of reperfusion arrhythmia and with the effect of verapamil on arrhythmia. In vivo study: Fifty anesthetized dogs were divided into two groups the control group (n = 37) and the verapamil group (n = 13). The left anterior descending coronary artery (LAD) was occluded for 15 min and then reperfused for 5 min. Physiological saline or verapamil (0.4 mg/kg) was infused 5 min prior to the LAD reperfusion. Eleven (30%) of the control dogs developed "reperfusion arrhythmia" (arrhythmia group) but 26 did not (non-arrhythmia group), while the verapamil group, none of the 13 dogs developed arrhythmia. Immediately after 5 min reperfusion, myocardial plasma membrane and mitochondria were prepared from the normal and the reperfused area. In the arrhythmia group, an increase in free fatty acids (FFA) and a decrease in phospholipids were observed in membrane samples, and the content of calcium in the mitochondria increased in the reperfused myocardium; these changes were not observed in the non-arrhythmia group or the verapamil group. In vitro study: In vitro study consisted of two experiments. In experiment 1, incubation of myocardial plasma membrane with phospholipase (PLase) A2 increased only the unsaturated FFA, while PLase C increased all the detected FFA. In experiment 2, the effects on myocardial membrane potentials induced by PLase A2 and PLase C were studied by using microelectrodes. Each PLase caused a decrease in the resting potential and the magnitude and duration of the action potential. These results and the fact that Ca++ is the essential factor which activates PLase suggest that the activation of PLase, triggered by Ca++ influx associated with reperfusion, develops the arrhythmogenic conditions, and that the protective effect of verapamil is based on inhibiting the activation of PLases by interfering with Ca++ influx.

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