The effect of streptomycin on stretch-induced electrophysiological changes of isolated acute myocardial infarcted hearts in rats†

Abstract

To explore whether the stretch of ischaemic myocardium could modulate the electrophysiological characteristics, especially repolarization via mechanoelectric feedback (MEF), as well as the effect of streptomycin (SM) on these changes. Methods Thirty-six wistar rats were randomly divided into four groups: control group (n = 9), SM group (n = 9), myocardial infarction (MI) group (n = 9), and MI + SM group (n = 9). After perfused on Langendorff, the isolated hearts were stretched for 5s by a ballon inflation of 0.2mL. After being stretched, the effect of the stretch was observed for 30s, including the 20, 20-70, 70, and 90% monophasic action potential duration (MAPD), i.e. MAPD(20), MAPD(20-70), MAPD(70), and MAPD(90), respectively, premature ventricular beats (PVB), and ventricular tachycardia (VT). Results The stretch caused a decrease in MAPD(20-70) (both P <0.01) and an increase in MAPD(90) (both P <0.01) in both control and MI groups. Moreover, the MAPD(90) in the MI group had increased more significantly than that in the control group (P <0.05). A concentration of 200 micromol/L of SM had no influence on both MAPD(20-70) and MAPD(90) of basic state (P > 0.05, except MAPD(20-70) between the control and SM groups, P < 0.01), whereas it had reduced the length of MAPD(90) (P < 0.05) and inhibited the decrease in MAPD(20-70) induced by the inflation. There was a decrease in the tendency of MAPD(70) after the stretch (P = NS) and SM had reversed the tendency, whereas MAPD(20) had no obvious changes after inflation. The incidence rate of PVB and VT in the MI group was higher than that in the control group after inflation (P < 0.01). The 200 micromol/L SM reduced the incidence rate of PVB, and obviously inhibited the occurrence of VT (P < 0.01). Stretch could alter the electrophysiological activities of myocardium via MEF, which could enhance in acute myocardial infarction and facilitate the generation and maintenance of malignant arrhythmias. SM could significantly inhibit the occurrence of arrhythmias, which may correlate with the effect on blocking stretch-activated ion channels.