Intravenous magnesium sulphate and reperfused myocardium: preservation of function and reduction of infarct size.

The aim of the study was to examine the effects of intravenous magnesium sulphate (MS) administration on myocardial contractile function and infarct size after occlusion of the left circumflex artery of the heart for 60 minutes. Under sodium pentobarbital anaesthesia (30 mg/kg. intravenously) the hearts of mongrel dogs (n = 13) were instrumented to measure left ventricular pressure (LVP), regional contractile function of the territories perfused by the left circumflex and anterior descending coronary arteries (%SS), mean arterial pressure (MAP), and coronary blood flow velocity (CFV). Immediately upon release of the coronary occlusion, either intravenous magnesium sulphate (100 mg/kg) or a dextrose vehicle (D5W) was infused. Animals were killed, their hearts excised and cut in 1 cm slices from apex to base and incubated in triphenyl tetrazolium chloride (TTC) for 20 minutes to measure infarcted areas. In the control group (n = 7), myocardial contractile function was severely depressed during the occlusion and displayed the same pattern of dysfunction during 3 h of reperfusion. The %SS of the area perfused by the circumflex artery at the end of the reperfusion period was 0.02 +/- 3 (mean + SEM) P < 0.05 vs MS; P < 0.05 vs pre-occlusion) and percentage of necrosis of the area at risk was 17.42 +/- 6 (P < 0.05 vs MS). In the magnesium sulphate group (n = 6), %SS was depressed during the occlusion as in the control group, but was preserved during reperfusion time, 9.8 +/- 1.0 (P < 0.05 vs D5W; P < 0.05 vs pre-occlusion) and showed significantly less percentage of necrotic tissue, 4.53 +/- 1 (P < 0.05 vs D5W). These results suggest that intravenous magnesium sulphate preserves myocardial contractile function and reduces infarct size significantly following a period of complete coronary occlusion.