内皮素-1对血管通透性的影响及一氧化氮的介导作用  被引量:4

Effect of endothelin-1 on vascular permeability via formation of nitric oxide

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作  者:李元义[1] 方之扬[1] 陈玉林[1] 

机构地区:[1]第二军医大学长海医院烧伤中心,上海200433

出  处:《中国病理生理杂志》1997年第6期706-709,共4页Chinese Journal of Pathophysiology

摘  要:应用大鼠脾、肾切除模型,观察内皮索-1对血管通透性的影响及一氧化氮的介导作用。结果发现:静脉恒速灌注内皮素-11h,平均动脉压和血球压积明显高于生理盐水对照组,血浆容量明显少于对照组,血浆蛋白漏出率和125I-白蛋白在心、肺和空肠组织的分布明显高于对照组。同时灌注一氧化氮合成酶抑制剂L-NMMA,虽然加强内皮素-1的升压作用,但明显减少内皮素-1引起的血浆蛋白漏出率增加,恢复血浆容量和血球压积,使125I-白蛋白在心、肺和空肠组织的分布较单用内皮素-1时明显减少。结果提示,内皮素-1组织选择性地增加血管通透性,这一作用是由一氧化氮介导的。The effect of endothelin -1 (ET - 1 ) on vascular permeability and mediating role of nitric oxide(NO) were investigated in splenectomized and nephrectomized rats. The results showed that intravenous infusion of ET - 1 produced a significant increase in mean arterial blood pressure(MAP)and hematocrit(Hct). This effect was associated with an increase in plasma albumin leakage, which was reflected by a marked reduction in plasma volume(PV). ET -- 1 enhanced albumin leakage primarily in heat, lung and empty intestine. L - NMMA, an inhibitor of NO systhase, inhibited the ET-1 induced rise in Hct, although it enhanced the ef- fect of ET - 1 on MAP significantly. Meanwhile, L - NMMA attenuated the ET - 1 - induced PV losses and albumin leakage ,and reduced the distribution of tis I - albumin in heat, lung and empty intestine. The present study demonstrated that ET - 1 increased Hot independent of splenic contraction by enhancing vascular permeability and iou of PV, and suggested that NO may mediate its action on permeability.

关 键 词:一氧化氮 内皮素 血管通透性 

分 类 号:R362[医药卫生—病理学]

 

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