Yan Su-hua, Hu He-sheng, Wang Le-xin, Xing Qi-chong, Cheng Wen-juan, Xue Mei
Department of Cardiology, Qianfoshan Hospital of Shandong Province, Jinan, 250014, China.
Clin Invest Med. 2008;31(4):E198-205. doi: 10.25011/cim.v31i4.4780.
To investigate the influence of angiotensin-converting enzyme inhibitor (ACEI) on cardiac innervation and inducible ventricular arrhythmias (VAs) in healed myocardial infarction (MI).
Left anterior descending coronary artery was ligated to induce MI in 30 rabbits. After oral captopril (10mg/kg/d) for 8 weeks, electrophysiological study was performed to evaluate the incidence of inducible VAs. RT-PCR and immunohistochemistry were used to measure the cardiac innervation.
Eight weeks after the operation, the incidence of inducible VAs in the MI-placebo group was higher (58.3%, 7/12) than in the sham operation group (16.7%, 2/12, P < 0.05). However, the incidence of inducible VAs in the MI-captopril group was lower (27.2%, 3/11) than in the MI-placebo group (P < 0.05). Proliferation and growth of nerve fibres in the MI-placebo group were mainly distributed at the periphery of the infarcted and perivascular regions of the myocardium. The density of nerve fibres increased in the MI-placebo group (3889+/-521 microm2/mm2) compared with the sham group (1727+/-304 microm2/mm2, P < 0.01) at the infarct border. In the MI-captopril group, the density of nerve fibres (3507+/-433 microm2/mm2) at the infarct border did not differ from that in the MI-placebo group (P=0.07). MI-induced abnormal nerve fibre distribution was partly restored by captopril treatment.
In this study, prolonged captopril treatment was effective in preventing VAs in healed MI, partly by attenuating the spatial heterogeneity of cardiac innervation.
探讨血管紧张素转换酶抑制剂(ACEI)对愈合心肌梗死(MI)心脏神经支配及诱发性室性心律失常(VAs)的影响。
结扎30只兔的左冠状动脉前降支以诱导MI。口服卡托普利(10mg/kg/d)8周后,进行电生理研究以评估诱发性VAs的发生率。采用逆转录聚合酶链反应(RT-PCR)和免疫组织化学法检测心脏神经支配情况。
术后8周,MI-安慰剂组诱发性VAs的发生率(58.3%,7/12)高于假手术组(16.7%,2/12,P<0.05)。然而,MI-卡托普利组诱发性VAs的发生率(27.2%,3/11)低于MI-安慰剂组(P<0.05)。MI-安慰剂组神经纤维的增殖和生长主要分布在梗死心肌周边及血管周围区域。梗死边界处,MI-安慰剂组神经纤维密度(3889±521μm²/mm²)高于假手术组(1727±304μm²/mm²,P<0.01)。MI-卡托普利组梗死边界处神经纤维密度(3507±433μm²/mm²)与MI-安慰剂组相比无差异(P=0.07)。卡托普利治疗部分恢复了MI诱导的异常神经纤维分布。
本研究中,长期卡托普利治疗对愈合MI预防VAs有效,部分原因是减弱了心脏神经支配的空间异质性。