Effect of phalloidin on electrophysiological changes induced by stretch of myocardial infarcted hearts in rats

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Author:
CAO Jun-Xian(Department of Cardiology, the First Hospital of Harbin Medical University, Harbin 150001, China)
FU Lu(Department of Cardiology, the First Hospital of Harbin Medical University, Harbin 150001, China)
XIE Rong-Sheng(Department of Cardiology, the First Hospital of Harbin Medical University, Harbin 150001, China)
LI Jia(Department of Cardiology, the First Hospital of Harbin Medical University, Harbin 150001, China)
DAI Ying-Nan(Department of Cardiology, the First Hospital of Harbin Medical University, Harbin 150001, China)
ZHU Li-Qun(Department of Cardiology, the First Hospital of Harbin Medical University, Harbin 150001, China)
HAN Ying(Department of Cardiology, the First Hospital of Harbin Medical University, Harbin 150001, China)
Journal Title:
ACTA PHYSIOLOGICA SINICA
Issue:
Volume 60, Issue 02, 2008
DOI:
Key Word:
cytoskeleton; microfilament; mechanoelectric coupling; action potentials

Abstract: The present study aimed to explore whether the stretch of ischemic myocardium could modulate the electrophysiologicalcharacteristics via mechanoelectric feedback (MEF), as well as the effect of phalloidin on the electrophysiological changes. Thirty-twoWistar rats were randomly divided into 4 groups: control group (n=9), phailoidin group (n=7), myocardial infarction (MI) group (n=9),MI + phalloidin group (n=7). The acute myocardial infarction (AMI) was conducted by ligation of the left anterior descending (LAD)coronary artery for 30 min in isolated rat heart. The volume alternation of a water-filled latex balloon in the left ventricle produced thestretch of myocardium. After perfused on Langendorff, the isolated hearts were stretched for 5 s by an inflation of 0.1, 0.2 and 0.3 mLseparately and the effect of stretch was observed for 30 s, including the left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), ±dp/dt max , monophasic action potential duration at 90% repolarization (MAPD9o), and occurrence of premature ventricular beats (PVB) and ventricular tachycardia (VT). The stretch caused an increase of MAPD90 in both control and MIrats (P<0.05, P<0.01). Moreover, MAPD90 in MI group increased more significantly than that in the control group at the same degreeof stretch (P<0.05, P<0.01). Phalloidin (1 μmol/L) had no effect on MAPD90 in basal state. After stretch, MAPD90 in phalloidin groupslightly increased but was not significantly different from that in the control group. However, phalloidin reduced MAPD90 in infarctedmyocardium, especially when △V=0.3 mL (P<0.05). The incidence rates of PVB and VT in MI group were higher than that in the controlgroup (both P<0.01). And there was no significant difference in the incidence rates of PVB and VT between phalloidin group and controlgroup. Phalloidin inhibited the occurrence of PVB and VT in infarcted hearts (both P<0.01). LVSP and +dp/dt max in MI group obviouslydecreased (P<0.01 vs control). With application of phalloidin, LVSP slightly, but not significantly increased in infarcted hearts, while-dp/dtmax significantly increased (P<0.05). It is suggested that MI facilitates the generation and maintenance of malignant arrhythmias,while phalloidin obviously inhibits the occurrence of arrhythmias.

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