MAGNESIUM - EFFECTS ON REPERFUSION ARRHYTHMIAS AND MEMBRANE-POTENTIALIN ISOLATED RAT HEARTS

The effects of Mg2+ concentration (Mg-0(2+), 0, 1.2, 2.4, and 4.8 mM) on the incidence of reperfusion arrhythmias and on the cellular electr ical activity were studied in spontaneously beating rat hearts. The su rface electrogram and the membrane potential were recorded in control conditions, during 10 min of regional ischemia (ligature of the left a nterior descending coronary artery), and on reflow. Changes in Mg-0(2) did not alter action potential morphology but the depolarization ind uced by ischemia decreased with increasing Mg-0(2+). In hearts perfuse d with Mg2+ free solution or 1.2 mM subthreshold delayed afterdepolari zations (DADs) were often detected during ischemia. Moreover, DADs cou ld be identified as initial events in the production of extrabeats or tachycardia appearing on reperfusion under these conditions. Chaotic e lectrical activity during fibrillation precluded the observation of DA Ds. The overall incidence (100%) and severity of ventricular tachyarrh ythmias (80% tachycardia and fibrillation) was similar in both groups. At high Mg-0(2+), subthreshold DADs were occasionally observed during ischemia and often on reperfusion where they did not lead to the deve lopment of overt arrhythmias. Consequently, the incidence, severity, a nd duration of arrhythmic episodes on reflow was markedly reduced. Rai sing Mg-0(2+) only on reperfusion did not prevent the development of a rrhythmias, whose morphology in the intracellular recordings was simil ar to that found in hearts perfused without Mg2+ or with 1.2 mM. The r ecovery of sinus rhythm after 10 min of reperfusion was linearly relat ed to Mg-0(2+). Our data strengthen the view that reperfusion arrhythm ias belong to the Ca2+ mediated non reentrant type and suggest that Mg 2+ counteracts these arrhythmias by depressing cytosolic Ca2+ oscillat ions. Besides, it appears that raising Mg-0(2+) reduces ischemic K-0() accumulation. The resulting changes in resting potential could contr ibute to lower DADs amplitude and thus decrease the arrhythmogenic pot ential of the Ca-i(2+), oscillations induced by reperfusion.