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首页> 外文期刊>Clinical and experimental hypertension: CEH >Improvement in the capillarity of the left ventricular wall of stroke-prone spontaneously hypertensive rats following angiotensin II receptor blockade.
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Improvement in the capillarity of the left ventricular wall of stroke-prone spontaneously hypertensive rats following angiotensin II receptor blockade.

机译:血管紧张素II受体阻断后,中风倾向性自发性高血压大鼠左心室毛细血管的改善。

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摘要

The effect of the angiotensin II type 1 receptor blockade, candesartan cilexetil (TCV116), on the capillarity of the innermost region of the left ventricular subendocardium were studied in stroke-prone spontaneously hypertensive rats (SHRSP). The rats were fed for 32 days on chow that contained TCV116, the average dose being 0.96 mg/kg/day. Compared with values from control SHRSP, the systolic blood pressure, left ventricular weight and cross-sectional area of cardiomyocytes decreased. A significant increase in the total capillary density was coupled with a decrease of capillary domain areas in all capillary portions. The proportion of venular capillary portions, which was low in control SHRSP, increased significantly, suggesting neoangiogenesis of capillaries. The results indicate that AT1-receptor blockade caused regression of the hypertrophied cardiomyocytes and improved capillarity of the left ventricular wall.
机译:在易发生中风的自发性高血压大鼠(SHRSP)中研究了血管紧张素II 1型受体阻断剂坎地沙坦酯(TCV116)对左心室内膜下层最内层毛细血管的影响。大鼠用含有TCV116的食物喂养32天,平均剂量为0.96 mg / kg /天。与对照SHRSP的值相比,收缩压,左心室重量和心肌细胞横截面积降低。总毛细血管密度的显着增加与所有毛细血管部分中毛细血管区域的减少有关。在对照SHRSP中较低的静脉毛细血管部分的比例显着增加,表明毛细血管的新血管生成。结果表明,AT1受体阻滞导致肥厚型心肌细胞消退并改善左心室壁的毛细血管。

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