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血管紧张素II可诱导正常及损伤大鼠动脉壁中的平滑肌细胞增殖。

Angiotensin II induces smooth muscle cell proliferation in the normal and injured rat arterial wall.

作者信息

Daemen M J, Lombardi D M, Bosman F T, Schwartz S M

机构信息

Department of Pathology, University of Limburg, Maastricht, The Netherlands.

出版信息

Circ Res. 1991 Feb;68(2):450-6. doi: 10.1161/01.res.68.2.450.

Abstract

The present study was undertaken to explore the possibility that neointimal smooth muscle cells, the characteristic cells of restenosis and atherosclerosis, are selectively stimulated to replicate by a hypertensive stimulus. Angiotensin II (AII) was infused by osmotic minipumps for 2 weeks in 4.5-month-old rats. Group A received AII (200 ng/min) 2 weeks after a balloon catheter-induced injury of the thoracic aorta and left common carotid artery. Group B received only AII, group C only balloon denudation, and group D neither balloon injury nor AII. During the AII or Ringer's solution infusion, all animals received [3H]thymidine via a second minipump to measure DNA synthesis. AII increased the systolic pressure by more than 40 mm Hg. AII significantly increased DNA synthesis in the media of the carotid artery from 0.2 +/- 0.2% in group C to 2.5 +/- 1.5% in group A (mean +/- SD, n = 5 or 6). DNA synthesis in the neointima of the carotid artery significantly increased with AII from 4.8 +/- 4.2% in group C to 19.8 +/- 13.9% in group A. Cross-sectional area of the neointima almost doubled during AII infusion, and it increased approximately 25% in the media. Comparable results were obtained in the aorta. In a second experiment, AII was infused (125 ng/min) for 2 weeks in 11-week-old rats. Concomitantly, [3H]thymidine was given. Control rats received Ringer's solution and [3H]thymidine in their pumps. Blood pressures were elevated to the same extent as in the older animals.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

本研究旨在探讨以下可能性

作为再狭窄和动脉粥样硬化特征性细胞的新生内膜平滑肌细胞,是否会被高血压刺激选择性地刺激进行复制。通过渗透微型泵在4.5月龄大鼠中输注血管紧张素II(AII)2周。A组在球囊导管诱导胸主动脉和左颈总动脉损伤2周后接受AII(200 ng/分钟)。B组仅接受AII,C组仅接受球囊剥脱,D组既不接受球囊损伤也不接受AII。在输注AII或林格氏液期间,所有动物通过第二个微型泵接受[3H]胸腺嘧啶核苷以测量DNA合成。AII使收缩压升高超过40 mmHg。AII使颈动脉中膜的DNA合成从C组的0.2±0.2%显著增加到A组的2.5±1.5%(平均值±标准差,n = 5或6)。随着AII的作用,颈动脉新生内膜中的DNA合成从C组的4.8±4.2%显著增加到A组的19.8±13.9%。在输注AII期间,新生内膜的横截面积几乎增加了一倍,中膜增加了约25%。在主动脉中也获得了类似的结果。在第二个实验中,在11周龄大鼠中输注AII(125 ng/分钟)2周。同时,给予[3H]胸腺嘧啶核苷。对照大鼠在其泵中接受林格氏液和[3H]胸腺嘧啶核苷。血压升高到与老年动物相同的程度。(摘要截断于250字)

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