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Journal of the Arab Society for Medical Research. 2013; 8 (1): 12-18
en Inglés | IMEMR | ID: emr-166962

RESUMEN

Acute myocardial infarction remains a leading cause of morbidity and mortality worldwide. The present study was carried out to investigate the possible protective effects of insulin, ATP, and [L]-arginine on cardiac dysfunction in experimental isoproterenol [ISO]-induced myocardial infarction [MI], aiming at achieving useful means for protection and therapy against MI. Wistar rats of both sexes were allocated into five groups: the control group, the untreated MI group, and MI groups treated with insulin, ATP, or [L]-arginine. All rats were subjected to ECG recording, and plasma levels of troponin I and triglycerides were determined. The isolated perfused hearts, according to Langendorff's preparation, were studied; the left ventricular weight [LV] was determined, and the LV per body weight ratio [LV/BW] was calculated. The percentage mortality and total arrhythmia were significantly reduced upon treatment with ATP and [L]-arginine. The ST segment elevation was significantly reduced in insulin-treated rats. The QRS duration and QT[o] intervals were significantly decreased in ATP-treated and [L]-arginine-treated rats, and the QT[c] interval was significantly shortened in all three treated groups. The levels of plasma triglycerides significantly reduced on treatment with insulin and ATP. In the three treated groups, the peak developed tension baseline value and maximal response were significantly increased when compared with the untreated group. In addition, the half-relaxation time baseline value was significantly decreased in the treated groups when compared with the control group. The myocardial flow rate baseline value and maximal response were significantly increased on [L]-arginine treatment. The LV weights and LV/BW ratios were significantly increased in all three treated groups. Insulin, ATP, and [L]-arginine were variably effective in partially modifying the ISO-induced MI insults and offered partial protection against ISO-induced myocardial damage

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