ABSTRACT
Objective To observe the protective effect of magnesium gluconate on myocardial apoptosis by ischemia reperfusion injury in isolated rat hearts, and study the possible mechanism. Methods The hearts of 48 Sprague-Dawely rats were isolated, linked to Lange-ndorff perfusion apparatus, and randomly divided into 3 equal groups(n = 16 each) : Control group, ischemia/reperfusion (I/R) group and magnesium gheonate group. 8 rats in each group were perfused. Control group was pedused with modified KH buffer for 110min. I/B group was perfuesd with modified KH buffer for 20 min, then exposed to iscbemia for 30 min, and then reperfused with modified KH buffer for 60 min. Magnesium gheonate group was perfumed with modified KH buffer with magnesium gluconate for 20 min, then exposed to isohemia for 30 min and then reperfused with modified KH buffer with magnesium glueonate for 60 min. Lacate dehydrogenase (LDH) and ereatine kinase (CK) in the effluent liquid from the heart were measured after reperfusion. The concentration of Ca2+ and NO in the left ventricle were determined. The other 8 rats in each group were reperfused for 120 minutes as the method described before. After repeffusion, the myoeyte apoptosis was examined by Annexin-V-FITC/PI. After the two experiments the incidence of ventrieular arrhytlunias during reperfusion was assessed. Results Compared with I/R, magnesium glueonate decreased the incidence of ventricular an'hythmias(P <0. 01). The contents of CK and LDH in the effluent liquid from the heart in magnesium glueonate group was lower than that of I/R group (P <0. 01). The contents of Ca2+ and NO in the left ventricle in magnesium gluconate group was decreased than that of I/R group (P <0. 01). The index of myocyte apoptosis were significanfly lower in magnesium glueonate group than that of I/R group (apoptosis index :27.79±1.59 vs 33.61±2.10, P < 0. 01) . Conclusion Magnesium glueonate has protective effect on myocardial isohemia reperfusion injury in rats. The protective effect may be related to decreasing myocyte apoptosis by increasing the content of NO and relieving calcium overload.