The effect of Mg L-asparaginate (Mg-L-Asp), Mg
chloride (
MgCl2) and Mg
sulfate (MgSO4) on the severity of
isoproterenol-induced myocardial injury in Mg-deficient rats has been evaluated. To induce Mg deficiency, twenty-eight rats were placed on a low Mg diet (Mg content < 15 mg/kg) and demineralized water for 10 weeks. Twelve control rats were fed a basal control diet (Mg content = 500 mg/kg) and water (with Mg content 20 mg/l) for equal duration. On day 49 of low Mg diet, Mg-deficient rats were randomly divided into four groups: 1) group that continued to receive low Mg diet; 2) low Mg diet plus oral MgSO4; 3) low Mg diet plus oral Mg-L-Asp and 4) low Mg diet plus oral
MgCl2 (50 mg of Mg per kg of
body weight).
Isoproterenol was injected subcutaneously (30 mg/kg BW, twice, at an interval of 24 hours) on the day 70 of the study, when plasma and erythrocyte Mg level in rats fed a low Mg diet were significantly decreased by 47% and 45% compared to intact animals. Twenty-four hours after second injection of
isoproterenol, tests for activities of
creatine kinase (CK),
lactate dehydrogenase (LDH) and
aspartate aminotransferase (AST) were run and histopathological study was carried out. Administration of
isoproterenol to rats resulted in significantly elevated plasma CK, LDH and AST, however analyses in Mg deficient group demonstrated more dramatically increased activity of CK and AST compared to control rats (3,06 and 4,67 fold in Mg-deficient group vs. 1,91 and 3,92 fold in intact group). Increased leakage of cardiac injury markers was concomitant to increased volume of fuchsinophilic cardiomyocytes (54.2 +/- 1.7% in Mg-deficient group and 38.9 +/- 1.9% in intact group, p < 0.05). However, pretreatment with of
MgCl2, MgSO4 and Mg-L-Asp during 21 days favorably decreased sensitivity of myocardium to
isoproterenol-induced ischemic injury. All evaluated
salts significantly decreased myocyte marker
enzymes as well as protected myocardium against
isoproterenol-induced histopathological perturbations.