生理学报
生理學報
생이학보
ACTA PHYSIOLOGICA SINICA
2001年
2期
128-132
,共5页
卢宁%田德志%周莉%姚泰%朱依纯
盧寧%田德誌%週莉%姚泰%硃依純
로저%전덕지%주리%요태%주의순
心肌梗塞%AT1A受体%AT2受体%免疫组化%心肌重构
心肌梗塞%AT1A受體%AT2受體%免疫組化%心肌重構
심기경새%AT1A수체%AT2수체%면역조화%심기중구
为探讨AT1、 AT2 受体在心肌重构演变过程中的作用, 本实验应用免疫组化、电镜技术和图像分析方法, 观察了大鼠心梗后心肌重构过程中非梗塞区AT1、 AT2受体表达的动态变化。结果显示, 心梗术后3 d, 电镜显示非梗塞区心肌细胞肌原纤维横纹消失, 线粒体肿胀, 成纤维细胞增多, 免疫组化显示AT1A受体在非梗塞区心肌组织表达明显升高(P<0.001), AT2受体表达无明显变化(P>0.05); 心梗术后14 d, 可见心肌细胞肌原纤维横纹, 心肌细胞间胶原纤维明显增多, 同时AT1A受体在心肌的表达比心梗术后3 d 时减弱, 但仍高于对照组(P<0.05), AT2受体表达明显增加(P<0.001)。结果提示: 心梗后非梗塞区心肌AT1A、 AT2受体表达先后上调, 可能参与介导心肌重构过程。
為探討AT1、 AT2 受體在心肌重構縯變過程中的作用, 本實驗應用免疫組化、電鏡技術和圖像分析方法, 觀察瞭大鼠心梗後心肌重構過程中非梗塞區AT1、 AT2受體錶達的動態變化。結果顯示, 心梗術後3 d, 電鏡顯示非梗塞區心肌細胞肌原纖維橫紋消失, 線粒體腫脹, 成纖維細胞增多, 免疫組化顯示AT1A受體在非梗塞區心肌組織錶達明顯升高(P<0.001), AT2受體錶達無明顯變化(P>0.05); 心梗術後14 d, 可見心肌細胞肌原纖維橫紋, 心肌細胞間膠原纖維明顯增多, 同時AT1A受體在心肌的錶達比心梗術後3 d 時減弱, 但仍高于對照組(P<0.05), AT2受體錶達明顯增加(P<0.001)。結果提示: 心梗後非梗塞區心肌AT1A、 AT2受體錶達先後上調, 可能參與介導心肌重構過程。
위탐토AT1、 AT2 수체재심기중구연변과정중적작용, 본실험응용면역조화、전경기술화도상분석방법, 관찰료대서심경후심기중구과정중비경새구AT1、 AT2수체표체적동태변화。결과현시, 심경술후3 d, 전경현시비경새구심기세포기원섬유횡문소실, 선립체종창, 성섬유세포증다, 면역조화현시AT1A수체재비경새구심기조직표체명현승고(P<0.001), AT2수체표체무명현변화(P>0.05); 심경술후14 d, 가견심기세포기원섬유횡문, 심기세포간효원섬유명현증다, 동시AT1A수체재심기적표체비심경술후3 d 시감약, 단잉고우대조조(P<0.05), AT2수체표체명현증가(P<0.001)。결과제시: 심경후비경새구심기AT1A、 AT2수체표체선후상조, 가능삼여개도심기중구과정。
Immunohistochemical and electron microscopic techniques and image analysis were employed to investigate the regulation of cardiac AT1A and AT2 subtype receptors in rats during cardiac remodeling following myocardial infarction (MI). Positive immunostaining for AT1A and AT2 receptors was observed in myocytes and vessels with AT1A being more than AT2. Three days after MI, disappearance of myocardial cross striation and fibroblast hyperplasia were found with electron microscopy. AT1A receptor protein expression in myocardial noninfarcted portion notably increased compared with that in sham-operated control rats (P<0.001). No apparent changes were observed in AT2 receptor (P>0.05). Two weeks after MI, myocyte cross striation and collagen deposition were found. Meanwhile, AT1A receptor staining decreased compared with that of three days after MI (P<0.01), but there was still more than that of the control (P<0.05). AT2 receptor was significantly increased compared with that of the sham-operated control rats (P<0.001). These results suggust that both AT1A and AT2 receptor protein expression was upregulated in noninfarcted myocardium after MI, and the regulation of AT1A and AT2 receptors after MI may be involved in post-infarction cardiac remodeling.