一氧化氮缺乏与高血压以及脑肾心组织损伤的研究  

Nitric oxide deficiency and hypertension and injuries of brain, kidney, and heart tissues

作　　者：张玉珍[1] 董寿祺[1] 顾德官[1] 蔡伟菁[1] 茅守玉[1] 龚兰生[1] 

机构地区：[1]上海第二医科大学附属瑞金医院上海高血压研究所

出　　处：《中国病理生理杂志》1998年第3期246-249,共4页Chinese Journal of Pathophysiology

摘　　要：目的和方法：给自发性高血压大鼠（ＳＨＲ）使用一氧化氮合酶竞争性拮抗剂Ｌ－ＮＮＡ后观察一氧化氮（ＮＯ）缺乏对高血压及脑肾心组织损伤的影响。结果：饲ｌ－ＮＮＡ的ＳＨＲ血压进一步升高，脑卒中发生显著增加，卒中率７８２５％，肾心缺血性病变明显加重，大鼠存活时间显著缩短；而对照ＳＨＲ无一例发生脑卒中，同时给予ＮＯ合成底物左型精氨酸（Ｌ－Ａｒｇ）脑卒中发生显著少于单饲Ｌ－ＮＮＡ，卒中率为２５％，Ｐ＜００５，肾心的缺血性病变也显著减轻，大鼠存活时间显著延长。结论：提示ＮＯ在调节ＳＨＲ血管张力，保证脏器血液供应。AIM and METHODS: To observed the effects of nitric oxide (NO) deficiency induced by nitric oxide synthase inhibitor, N G -nitro-L-arginine (L-NNA) on blood pressure (BP) and injuries of brain, kidney and heart tissues in SHR.RESULTS: In SHR treating with L-NNA, blood pressure was significantly increased, storke occurrence also increased (the rate was 78 25%, while there was no stroke in control SHR, P <0 01),pathological changes of heart and kidney were produced markedly, and the living time of rats decreased. In SHR cotreated with L-NNA and L-arginine, the substrate of NO synthesis, decreased significantly stroke rate reduced(25%, P <0 05) injuries of kidney and heart,and the living time of rats prolonged compared with SHR treated only with L-NNA. CONCLUSION:These data demonstrated that NO played a crucial role in regulating vascular tension, ensuring enough blood supply for organs in SHR and L-Arg could alleviate L-NNA-exacerbated severe pathological changes of hypertensive target organs.

关 键 词：一氧化氮 脑血管意外 高血压 大鼠 肾组织损伤 心肌损伤 

分 类 号：R544.1[医药卫生—心血管疾病] R743.3[医药卫生—内科学]