Effects of substance P on left ventricular functions in rats with acute myocardial infarction

Objective To investigate the role of substance P(SP) in the regulation of left ventricular functions in acute myocardial infarction rats. Methods Forty-eight Sprague-Dawley male rats weighing 250-300 g,were assigned into in vivo and in vitro experiments.The models of acute myocardial infarction in vivo and in vitro were carried out by ligating the left anterior descending coronary artery.Sham-operated rats underwent the identical surgical procedure except that the suture was not tightened around the coronary artery.The rats were divided into three groups in two experiments respectively:sham group,coronary artery occlusion(CAO) group and D-SP group or SP group.The rats in D-SP group and SP-CAO group were pretreated with a specific antagonist of NK-1 receptor(D-SP,10-7 mol/L,1 ml/kg,intravenous injection,at 15 min before CAO,in vivo) and SP(10-6 mol/L,administrated continuously for 15 min before CAO,in vitro),respectively,while the rats in sham group and CAO group were given the same volume of physiological saline as scheduled.Electrocardiograms and intra-ventricular pressures were monitored during the study.Left ventricular systolic pressure(LVSP),left ventricular end-diastolic pressure(LVEDP),the maximum rise rate of left ventricular pressure(LV+dP/dtmax),the maximum descending rate of left ventricular pressure(LV-dP/dtmax) and heart rate(HR) were continuously recorded.Left ventricular development pressure(LVDP) was calculated(=LVSP-LVEDP). Results Pretreatment with D-SP in in vivo rats significantly increased LV+dP/dtmax and decreased LV-dP/dtmax after CAO(P0.05).Pretreatment of the isolated CAO hearts with SP significantly increased LVEDP(P0.05).SP or D-SP produced no effects on HR after CAO(P0.05). Conclusion SP could attenuate left ventricular systolic and diastolic functions after acute myocardial infarction in rat heart by activating NK-1 receptor.