Abstract: Objective： To investigate the effect of captopril, an angiotensin converting enzyme inhibitor, on cardiac neural remodeling after myocardial infarction. Methods： Forty-two rabbits were randomly divided into three groups: the captopril group, receiving ligation of the left anterior descending branch with captopril administration（10mg/kg·d）; the control group, receiving ligation of the left anterior descending branch; and the sham group, receiving thoracotomy without ligation. After 8 weeks, electrophysiological recordings were carried out and expressions of S100, GAP43 and TH were determined by immunohistochemical technique or RT-PCR. Results： The incidence of inducible VAs in the control group was obviously higher than that in the sham group (P＜0.01) after 8 weeks. However, it was significantly decreased after captopril treatment(P＜0.01). The densities of S100 and GAP43 positive nerve fibers were significantly greater in the control group than distribution in the control group was obviously diverse in contrast to the sham group. After captopril treatment, the densities dropped compared to the control group（P=0.07, P=0.13）. Otherwise, captopril normalized the inhomogeneous distribution and abnormal appearance of nerve fibers. The densities of S100 and GAP 43 positive nerve fibers at the non-infarct left ventricular free wall were decreased after captopril treatment, but no significant differences were found（P＞0.05）. Expression of TH mRNA in the control group was significantly increased compared with the sham group at both the infarct border and the noninfarct left ventricle free wall. However, no significant differences were found between the captopril group and the control group. Conclusion： Captopril treatment is effective in reducing the occurrence of VAs in healed MI, partly by attenuating the heterogeneity of cardiac innervation and normalizing the appearance of cardiac nerve fibers.

Key words: Myocardial infarction, Cardiac remodeling, Captopril, Ventricular arrhythmia