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

Aims To explore whether the stretch of ischaemic myocardium could modulate the electrophysiological characteristics, especially repolarization via mechanoetectric 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 Ml + SM group (n = 9). After perfused on Langen-dorff, the isolated hearts were stretched for 5 s by a ballon inflation of 0.2 mL. After being stretched, the effect of the stretch was observed for 30 s, 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 MAPD20-70 (both P < 0.01) and an increase in MAPD90 (both P < 0.01) in both control and Ml groups. Moreover, the MAPD90 in the Ml group had increased more significantly than that in the control group (P < 0.05). A concentration of 200 mu mo/L of SM had no influence on both MAPD20-70 and MAPD(90) of basic state (P > 0.05, except MAPD20-70 between the control and SM groups, P < 0.01), whereas it had reduced the length of MAPD90 (P < 0.05) and inhibited the decrease in MAPD20-70 induced by the inflation. There was a decrease in the tendency of MAPD70 after the stretch (P = NS) and SM had reversed the tendency, whereas MAPD20 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 mu mol/L SM reduced the incidence rate of PVB, and obviously inhibited the occurrence of VT (P < 0.01). Conclusions 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.