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首页> 外文期刊>International Journal of Cardiology >Angiotensin II type 1 receptor blockade in the prevention of in-stent restenosis: systemic versus local delivery.
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Angiotensin II type 1 receptor blockade in the prevention of in-stent restenosis: systemic versus local delivery.

机译:血管紧张素II 1型受体阻滞剂预防支架内再狭窄:全身性递送与局部递送。

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摘要

We have read with great interest the article by Groenewegen et al. entitled 'Effects of angiotensin II and angiotensin II type 1 receptor blockade on neointimal formation after stent implantation' [1]. In that article, the authors evaluated the effect of supraphysiologic levels of angiotensin II and selective angiotensin II type 1 receptor (ATI-receptor) blockade on neointimal formation and systemic endothelial function after stent implantation in the rat abdominal aorta. They found that candesartan cilexetil treatment did not result in reduction of neointimal area and did not reduce neointimal thickness compared to the control group. Also candesartan had no effect on endothelial function [1]. They concluded that supraphysiologic levels of angiotensin II aggravate neointimal formation in the stented rat abdominal aorta, and in parallel decreases endothelial function. ATI-receptor blockade does not reduce neointimal formation in rats without supraphysiologic angiotensin II levels.
机译:我们非常感兴趣地阅读了Groenewegen等人的文章。题为“血管紧张素II和1型血管紧张素II受体阻滞对支架植入后新内膜形成的影响” [1]。在那篇文章中,作者评估了在大鼠腹主动脉支架植入后,超生理水平的血管紧张素II和选择性血管紧张素II 1型受体(ATI受体)阻滞对新内膜形成和系统内皮功能的影响。他们发现,与对照组相比,坎地沙坦西酯治疗不会导致新内膜面积的减少,也不会减少新内膜的厚度。坎地沙坦对内皮功能也没有影响[1]。他们得出的结论是,血管紧张素II的超生理水平会加重支架大鼠腹主动脉中的新内膜形成,并同时降低内皮功能。没有超生理学血管紧张素II水平的大鼠,ATI受体阻滞剂不会减少新内膜的形成。

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