ncreased expression of cardiac angiotensin II type 1 ( AT ) receptors 1 decreases myocardial microvessel density after experimental myocardial infarction
ncreased expression of cardiac angiotensin II type 1 ( AT ) receptors 1 decreases myocardial microvessel density after experimental myocardial infarction
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发表时间：
2003
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通讯作者：
A. Boer;Y. Pinto;A. Suurmeijer;S. Pokharel;E. Scholtens;Michael Humler;J. Saavedra;F. Boomsma;W. H. Gilst;D. J. Veldhuisen
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作者：
A. Boer;Y. Pinto;A. Suurmeijer;S. Pokharel;E. Scholtens;Michael Humler;J. Saavedra;F. Boomsma;W. H. Gilst;D. J. Veldhuisen
目的：目的：研究心肌血管紧张素Ⅱ 1型（AT）受体水平升高对心肌梗死（MI）后微血管生长的影响。我们使用Sprague-Dawley（SD）大鼠作为对照。用选择性AT受体阻断剂11氯沙坦（Los）处理一些大鼠。3周后处死大鼠。结果：MI引起SD和TGR的左室肥厚和左室功能障碍，AT受体阻断剂可阻止MI的发生。MI使非梗死区心肌微血管密度降低（SD MI：1653637/mm，P < 0.01），而2 2 TGR伴MI组微血管密度降低更明显（1298633/mm，P < 0.01）。AT受体阻断恢复了微血管密度（SD MI Los：2046 ± 6195/mm ; 1 ± 2 TGR MI Los：1742 ± 647/mm ; P，0.01，与未治疗相比）。校正左心室肥大后，微血管密度的差异仍然存在。AT受体阻断后微血管密度的增加并不伴随着心肌血管内皮生长因子（VEGF）水平的增加。微血管密度与左室舒张末期压（20.681，P，0.001）和N-ANP（20.424，P50.01）等心肌牵张参数相关。结论：心肌梗死后微血管密度下降时，AT 1受体过表达，这是服从AT受体阻断剂。这表明MI 11后AT受体阻断剂的功效可能不仅是由于LV重塑的减弱，而且还由于对血管生成的刺激作用。2003年欧洲心脏病学会。由Elsevier Science B. V.出版，版权所有。
Objective: To study the effects of increased levels of myocardial angiotensin II type 1 (AT ) receptor on microvascular growth 1 following myocardial infarction (MI).Methods: MI was created in transgenic rats (TGR) with a cardioselective overexpression of the AT receptor. We used Sprague–Dawley (SD) rats as controls. Some of the rats were treated with the selective AT receptor blocker 1 1 losartan (Los). Rats were sacrificed after 3 weeks. Results: MI caused left ventricular (LV) hypertrophy and LV dysfunction in both SD and TGR, which was prevented by AT receptor blockade. Furthermore, MI decreased microvessel density in the non-infarcted 1 2 myocardium (SD MI: 1653 637/mm ,P,0.01 vs. sham-operated controls), however, microvessel density decreased significantly more in 2 2 TGR with MI (1298633/mm ,P,0.01 vs. SD MI). AT receptor blockade restored microvessel density (SD MI Los: 2046 6195/mm ; 1 2 TGR MI Los: 1742647/mm ; P,0.01 vs. untreated). The differences in microvessel density were still present after correction for LV hypertrophy. The increase in microvessel density after AT receptor blockade was not accompanied by increased myocardial vascular 1 endothelial growth factor (VEGF) levels. Microvessel density correlated with parameters of myocardial stretch, such as LV end-diastolic pressure ( 20.681, P,0.001) and N-ANP ( 20.424, P50.01). Conclusions: Microvessel density after MI is decreased when the AT 1 receptor is overexpressed, and this is amenable to AT receptor blockade. This suggests that efficacy of AT receptor blockers post-MI 1 1 may not only be due to attenuation of LV remodeling, but also to a stimulatory effect on angiogenesis. 2003 European Society of Cardiology. Published by Elsevier Science B.V. All rights reserved.