Effects of post-treatment electroacupuncture on ventricular monophasic action potential and cardiac function in a rat model of ischemia/reperfusion injury

Abstract

Background: To determine the effects of post-treatment electroacupuncture (EA) on the electrophysiological properties of ventricular muscle in rats with ischemia/reperfusion (IR) injury. Methods: Male Sprague–Dawley (SD) rats were randomly assigned into sham-operated (SH), IR and IR + EA groups ( n = 8 each). The IR model was generated by ligation of the left anterior descending (LAD) coronary artery for 30 min. After establishing the IR model, EA was administered at PC6 for 30 min while opening the coronary artery and allowing reperfusion for 30 min. Heart rate (HR), mean arterial pressure and monophasic action potential (MAP) of cardiac muscle in the outer membrane of the antetheca of the left ventricle before coronary artery ligation ( T0), after coronary artery ligation for 30 min ( T1) and after reperfusion for 30 min ( T2) were recorded. At the same time, ventricular electrophysiological parameters including ventricular effective refractory period (ERP), conduction velocity (CV) and ventricular fibrillation threshold (VFT) were measured. Then, the cardiac function and the levels of creatine kinase-muscle/brain (CK-MB) and cardiac troponin I (cTnI) were monitored. Based on these data, monophasic action potential amplitude (MAPA), the maximum depolarization velocity ( Vmax) and the MAP durations at 50% and 90% repolarization (MAPD50 and MAPD90) were calculated to determine the incidence of arrhythmia during reperfusion. Results: Compared with the SH group, the IR group showed an obviously decreased HR as well as reduced mean arterial pressure, Vmax, CV, ERP and MAPA. All indices of cardiac function except left ventricular end-diastolic pressure (LVEDP) decreased (i.e. ventricular systolic pressure (LVSP), left ventricular ejection fraction (LVEF), fractional shortening (FS) and rate of the ventricular pressure rise/drop (±dp/dt)). Furthermore, the MAPD50 and MAPD90 were prolonged, and the levels of CK-MB and cTnI increased ( p < 0.05). In comparison to the IR group, HR and the mean arterial pressure were increased. All indices of cardiac function except LVEDP increased (LVSP, LVEF, FS and ±dp/dt). Vmax, CV, ERP and MAPA were also increased in the IR + EA group. However, MAPD50 and MAPD90 were distinctly shortened, and the levels of CK-MB and cTnI decreased ( p < 0.05). There were no statistically significant differences in VFT between the three groups ( p > 0.05). Conclusion: EA post-treatment can relieve prolongation of repolarization and slowed depolarization of ventricular muscle during IR, thus decreasing the rate of incidence of reperfusion arrhythmia.