一氧化氮缺乏诱导的高血压及心血管重构

Hypertension and cardiovascular remodeling induced by the deficiency of nitric oxide

目的 建立一氧化氮（NO）缺乏所致的高血压、心血管重构的动物模型。方法 Wistar大鼠，经饮水给予NO合酶抑制剂。对照组（C组）：仅给予饮水；NO合酶抑制剂组（L组）：L－NAME50mg／kg．d。每2周监测血压一次（尾袖法），8周后，颈动脉插管测定颈动脉压，摘取心脏，测定心脏湿重及室壁厚室，用病理结合体视学方法测定心肌细胞大小、血管中膜厚度、血管周围纤维化程度、管壁厚度／腔径比、管壁面积／腔径等心血管重构指标。结果 L组大鼠血压明显升高、心血管系统出现明显重构改变。结论 本研究证实，抑制NO合成可建立高血压和心血管重构的动物模型。

Objective To establish the animal model induced by chronic administration of L－NAME on hypertension and cardiovascular remodeling． Methods Male normotensive Wistar－Kyoto rats n＝32 were divided into four groups and given different drugs via drinking water for 8 weeks． Group C n＝10 received only tap water group L n＝10 L－NAME 50 mg／kg．d． Tailcuff blood pressure BP was measured every two weeks． After 8 weeks arterial pressure was measured and blood was collected through carotid artery． Then the hearts were removed、weight measured、the ratio of left ventricular mass LVM to the body mass BM and mean left ventricular wall thickness LVWT were determined． Pathologic and stereologic measurements were used in the following items the diameter of cardiac myocyte the lume R and wall area WA of small artery WA／R ratio and the degree of vascular fibrosis． Results Compared with other groups group L had higher systolic blood pressure LVM／BM and mean LVWT which proved the development of left ventricular hypertrophy LVH． Conclusion The study confirm that inhibiting NO production can lead to hypertension and cardiovascular remodeling．