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目的探讨在高脂饮食后动脉粥样硬化兔腹主动脉手术缩窄近端(高血压)与远端(低血压)血管中膜平滑肌组织血管紧张素Ⅱ(AngⅡ)的变化及相互关系。方法25只新西兰大白兔随机分为单纯手术组(C组,n=10)、高脂手术组(HC组,n=10)、高脂假手术组(SH组,n=5),饲养28周后,行腹主动脉缩窄术。术后继续饲养4周,在测量腹主动脉狭窄近端与远端血管压力后获取标本。采用HE染色检测血管中膜厚度,免疫组织化学分析检测中膜平滑肌细胞数量及AngⅡ水平。结果C组与HC组血管狭窄近端血压都比远端高[血压,C组近端(72.3±13.4)比远端(54.1±11.0)mmHg,P=0.001;HC组近端(84.2±5.3)比远端(52.6±5.9)mmHg,P=0.001],HC组近远端血压差值与C组相较增加100%(32比16mmHg)。C组与HC组狭窄近端中膜厚度都比远端高[中膜厚度,C组近端(144.9±4.9)比远端(133.9±8.3)μm,P>0.05;HC组近端(204.7±8.3)比远端(140.1±1.3),P=0.001]。AngⅡ水平狭窄近端比远端高[C组(0.11±0.01)比(0.08±0.02)μm-1,HC组(0.21±0.01)比(0.15±0.01)μm-1),HC组近-远端AngⅡ浓度差也比C组多100%(0.06比0.03)。结论单纯动脉狭窄引起的狭窄近远端压力差,不是引发动脉内膜中膜肥厚,α肌动蛋白增加,血管组织内AngⅡ增加的原因。只有在高脂高压同时影响下,血管狭窄近端的中膜才比狭窄远端增厚,而且伴有组织AngⅡ水平增高。
Objective To investigate the changes and relationships of angiotensin Ⅱ (Ang Ⅱ) in the proximal and distal hypertensive rats with atherosclerosis and abdominal aorta surgery. Methods Twenty - five New Zealand white rabbits were randomly divided into three groups: the surgery group (C group, n = 10), the hyperlipidemic surgery group (HC group, n = 10), the sham operation group (SH group, n = 5) Weeks, the abdominal aortic constriction surgery. After 4 weeks of continuous feeding, samples were obtained after measuring the proximal and distal vascular pressure of abdominal aortic stenosis. The thickness of vascular intima was detected by HE staining. The number of smooth muscle cells and the level of AngⅡ were detected by immunohistochemistry. Results The proximal blood pressure of vascular stenosis in group C and HC were higher than those in distal group [blood pressure, group C (72.3 ± 13.4) vs group (54.1 ± 11.0) mmHg, P = 0.001; group HC 84.2 ± 5.3 ) Than the distal end (52.6 ± 5.9) mmHg, P = 0.001]. The difference of blood pressure in proximal and distal HC group was increased by 100% (32 vs 16mmHg) compared with that of C group. The proximal medial thickness of stenosis was significantly higher in the C and HC groups than in the distal end (MED, 144.9 ± 4.9 vs 133.9 ± 8.3 μm, P> 0.05) ± 8.3) than the distal end (140.1 ± 1.3), P = 0.001]. The level of AngⅡ was higher in the proximal part of the stenosis than in the distal part of the HC group (0.11 ± 0.01 vs 0.08 ± 0.02 μm-1, 0.21 ± 0.01 vs 0.15 ± 0.01 μm-1) The difference in Ang Ⅱ concentration was also 100% more than in group C (0.06 vs. 0.03). Conclusions The narrowing of proximal and distal stenosis caused by simple arterial stenosis is not the reason of inducing intimal hyperplasia of the artery, increasing of α-actin and increasing of AngⅡ in blood vessels. Only under the influence of high-fat and high-pressure, the neointima near the stenosis is thicker than the stenosis, and the level of AngⅡ is increased.