目的 探讨心肌梗死(MI)后心脏局部是否存在区域性失神经支配现象,评价失神经支配对局部心室功能的影响.方法 将14只犬随机分为MI组与假手术对照组,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周应用程序刺激技术评价梗死区对应的远端心尖侧是否存在失神经支配现象;应用超声造影检测该部位组织血流情况,应用组织多普勒超声检测该部位心室功能.结果 MI组梗死区近端心底侧的非梗死区及正常对照组各部位在星状神经节刺激后ERPs值显著缩短,而远端心尖侧的非梗死区ERPs值在星状神经节刺激前后无明显变化,说明MI组心尖侧缺少神经支配.与正常对照组相比,MI组心底及心尖侧的组织运动速度均有所降低,但心尖侧较心底侧降低的比率[(心底侧-心尖侧)/心底侧]却显著大于正常对照组,而超声造影测定的造影剂峰值强度心尖侧较心底侧降低的比率较对照组无显著差异.结论 MI后心脏局部存在区域性失神经支配现象;交感神经缺失影响心肌局部组织运动功能.
Objective To investigate whether myocardial infarction(MI) can cause heterogeneity of sympathetic innervation and to evaluate the effects of denervation on focal ventricular function. Methods Randomly treated with ligating the left anterior descending coronary artery or sham - operation procedure, 14 canines were divided into infarction group and control group. Programmed ventricular stimulation was used to identify sympathetic denervation in noninfarcted myocardium apical to the infarction 4 weeks after infarction. Myocardial contrast echocardialgraphy (MCE) was executed on there, and the focal myocardium microvascular perfusion was detected. Doppler tissue imaging( DTl ) was used to evaluate regional ventricular function. Results Shortening of ERP values in response to sympathetic stimulation was presented at all regions of control group but only appeared at the base of the heart in the MI group and there was no significant difference at the apical of the .heart before and after sympathetic stimulation, which identified extensive denervation in the left ventricle below the infarct. The systolic velocity and diastolic velocity at both apical and basal regions to the infarction were lower than those in the controal group, But the apical decline proportion compared to the base [ (base- apex)/base] was greater than that in the controal group;As for peak intensity(H) of microbubbles detected by MCE, there was no significant difference of the apical decline proportion compared to the base [ ( base - apex)/base ] between MI group and controal group. Conclusion Regional denervation occurs after MI; Sympathetic denervation may contribute to the dysfunction of regional myocardium after MI.