中文摘要：

目的 探讨心肌梗死后是否存在区域性自主神经分布不均现象，评价交感神经刺激对心脏不同区域心室复极的影响。方法将14只犬随机分为心肌梗死组（7只）与假手术对照组（7只），心肌梗死组手术结扎冠状动脉前降支主干造成左心室前侧壁心肌梗死模型。术后4周应用程序刺激测定梗死区近端心底部及远端心尖部梗死比邻部位的有效不应期（ERP），假手术对照组取心肌梗死组对应部位进行检测。刺激左星状神经节后重复测定上述部位的ERP。应用免疫组织化学技术检测电生理电极所在部位的交感神经支配情况。结果心肌梗死组未给予左星状神经节刺激时，梗死区近端心底部的梗死比邻部位ERP值（162ms±9ms）与梗死区远端心尖部的梗死比邻部位ERP值（161ms±6ms）相比，差异无统计学意义（P〉0．05），这与假手术对照组相似（162ms±10ms比164ms±5ms，P〉0．05）；但在给予交感神经刺激后，仅心肌梗死组心尖部位的ERP值无明显变化，其他被测区域均出现ERP值缩短现象，心肌梗死组呈现心底部（141ms±10ms）与心尖部（157ms±8ms）之间心室复极离散（P〈0．05）。心肌梗死组心尖部电极所在部位交感神经免疫组织化学染色阴性，心底部及假手术对照组均可见正常的免疫染色阳性的神经纤维分布。结论心肌梗死后心脏局部存在区域性失神经支配现象；自主神经异常分布导致神经刺激后心室复极离散的发生。

英文摘要：

Objective To investigate whether myocardial infarction （MI） causes heterogeneity of sympathetic innervation and to evaluate the effects of sympathetic stimulation on myocardial repolarization in the regions of denervation after MI. Methods Fourteen dogs were randomly divided into 2 equal groups ： MI Group, undergoing ligation of the left anterior descending coronary artery, and Control Group, undergoing sham operation. Four weeks later thoracotomy was performed for the second time, the effective refractory period （ERP） of the non-infarcted myocardium at the base of heart proximal to the infracted myocardium and the ERP of the non-infarcted myocardium at the cardiac apex distal to the infarcted myocardium by S1S2 programmed stimulation. Then the left satellite ganglion was exposed, ligated, cut, and stimulated at the proximal end, and ERP was determined at the above mentioned regions again. After the ERP measurement the heart was taken out to undergo immunohistochemistry to observe the distribution of tyrosine hydroxylase （TH） positive nerve fibers. Results The ERP of the non-infarcted myocardium at the base of heart proximal to the infracted myocardium was not significantly different from that of the non-infarcted myocardium at the cardiac apex distal to the infarcted myocardium before sympathetic stimulation in both groups. In MI Group, however, the ERP of the non-infarcted myocardium at the base of heart proximal to the infracted myocardium was significantly shortened after stimulation at the satellite ganglion （ 141 ms±10 ms ） in comparison with that before the stimulation （ 162 ms±9 ms, P 〈 0.01 ） ; and the ERP of the non-infarcted myocardium at the cardiac apex distal to the infarcted myocardium after sympathetic stimulation （ 157 ms± 8 ms） was not significantly different from that before sympathetic stimulation （161 ms±6 ms）, however, was significantly longer than that of the non-infarcted myocardium at the base of heart proximal to the infracted myocardium （P〈0.05 ?