目的研究心肌梗死(MI)后心脏局部不同部位的β受体分布情况。方法 14只健康杂种犬,随机分为 MI 组(7只)与假手术对照组(7只),结扎冠状动脉前降支造成 MI 模型。术后4周应用组织多普勒超声技术检测梗死区近端心底部及远端心尖部与梗死区比邻的非梗死区心肌组织运动速度,静脉推注美托洛尔后重复测定,观察β受体阻滞剂对上述部位组织运动的抑制作用;应用RT-PCR 技术检测上述部位β_1、β_2受体 mRNA 表达情况。结果 MI 组心底及心尖侧的组织运动速度比正常对照组均有所降低,β受体阻滞剂干预后组织运动的抑制作用低于正常对照组,在心尖部尤其明显,可见该部位β受体密度减低。RT-PCR 显示 MI 组心底部及心尖部β_1受体 mRNA 表达量(0.78±0.02、0.41±O.02)低于正常对照组(0.82±0.03、0.85±0.04),心底部降低程度明显低于心尖部,差异有统计学意义(P<0.05);正常对照组心底与心尖之间的表达量无统计学差异。β_2受体的mRNA 表达量无显著变化。结论 MI 后心脏局部存在β_1受体 mRNA 表达量的区域性变化,而β_2受体无明显异常,这就造成心尖部β_1、β_2受体比例发生明显改变。
Ventricular remodeling （VR） after myocardial infarction （MI） makes a full impact on left ventricular dilation and dysfunction, severe arrhythmias and even sudden death. Thus it is very interesting and instructive to study the underlying regulatory mechanism for VR. Recently, evidenceI suggests that tumor necrosis factor-α （TNF-α） activity can independently influence VR, and aggravate myocardial dysfunction and cell death in the ventricle. The activation of pro-TNF〈t is adjusted by a disintegrin metalloproteinase （ADAM） 10 and ADAM17, the latter might take part in extracellular matrix （ECM） modulation in the borderline region of cardiac infarction.2 However, little is known about the relationship between ADAMsl0, 17 expressions and TNF-α activity in the process of VR after MI. The present study tested the hypothesis in rats that the interaction between ADAMsl0, 17 expressions and TNF-α activity was a contributory mechanism for VR of the healing myocardium, and metoprolol treatment might ameliorate VR inhibiting the mechanism.
