Externalization and internalization of cardiac endothelin receptors during different phases of sepsis in rat.

Objective. To study the redistribution ofendothelin- 1 (ET- 1 ) receptors in two subcellular organelles, the sarcolemreal membrane and the light vesicle, of rat heart during the progression of sepsis. Methods. Sepsis was induced by cecal ligation and puncture (CLP). ET1 receptor was assayed by using[125I]-ET1 binding. Marker enzyme activities, protein yield, and dry-to-wet weight ratio of cardiac membraneswere measured. Results. Septic rat heart exhibited two distinct phases: an initial hyperdynamic phase( 9h after CLP; early stage of sepsis) followed by a hypodynamic ( 18h after CLP, late stage of sepsis) phase. [125I]-ET1 binding study showed that during early stage of sepsis, the Bmax of ET1 receptors was increased by 30% in sarcolemma but decreased by 19% in light vesicles, while during late stage of sepsis, the Bmax was decreased by 24% in sarcolem-ma but increased by 38% in light vesicles. The total binding of sarcolemma and light vesicles was increased by 25% during early stage of sepsis but decreased by 17% during late stage of sepsis. Conclusions. These data indicated that ET1 receptors in the rat heart were externalized from light vesicles to sarcolemmal membranes during early hyperdynamic phase while internalized from surface membranes to intracellu-lar compartment during late hypodynamic phase of sepsis.     

扩血管药物治疗肺心病肺动脉高压的评价

正常人静息时平均肺动脉压为10～14 mmHg,平均肺动脉压超过20mmHg者称为肺动脉高压.肺动脉高压是肺心病发生发展的病理生理基础,其脉压高低是影响肺心病患者预后的重要因素之一,因此防治肺动脉高压对延缓肺心病的发生发展和降低病死率具有重要意义.     

巴曲酶的扩血管作用及其机制探讨

目的研究巴曲酶对血管张力的影响及其可能机制。方法离体大鼠主动脉环测定张力，主动脉薄片孵育测定ＮＯ生成、血管一氧化氮合酶（ＮＯＳ）活性与Ｌ－精氨酸（Ｌ－Ａｒｇ）转运。结果巴曲酶（０．１～２０Ｂｕ·Ｌ－１）浓度依赖性扩张大鼠离体主动脉环，去内皮血管对巴曲酶的舒张反应明显低于内皮完整血管（Ｐ＜０．０１），最大舒张反应分别为４０．１％±２１．９％和８８．１％±４．２％（Ｐ＜０．０１）。巴曲酶（１０Ｂｕ·Ｌ－１）刺激孵育主动脉产生ＮＯ－２增加１２８％（Ｐ＜０．０１），固有型ＮＯＳ（ｃＮＯＳ）和总ＮＯＳ（ｔＮＯＳ）活性分别增加２．０倍和４０．０％（Ｐ值均小于０．０１），诱导型ＮＯＳ（ｉＮＯＳ）活性无显著变化（Ｐ＞０．０５）。血管壁对Ｌ－Ａｒｇ的转运呈高和低亲和两种方式，巴曲酶（１０Ｂｕ·Ｌ－１）可使其最大转运速率Ｖｍａｘ分别增加８３．８％和４７．４％（Ｐ＜０．０１）。结论巴曲酶的内皮依赖的扩血管作用通过Ｌ－Ａｒｇ／ＮＯ途径，巴曲酶增加血管壁Ｌ－Ａｒｇ的转运和激活ＮＯＳ，使ＮＯ生成增加     

血管损伤影响离体平滑肌细胞增殖与钙稳态有关

本实验采用球囊剥脱术在体损伤血管，于术后３天和１０天取出血管做平滑肌细胞培养。结果发现，血管损伤后血管平滑肌细胞增殖活性显著增加，ＤＮＡ和蛋白质合成加速，细胞数目增多。在血管平滑肌细胞增殖过程中，钙内流增加，胞内钙含量升高。应用１０μｍｏｌ·Ｌ￣（－１）异搏定不但对钙稳态变化有一定的抑制作用，而且还对血管损伤诱导的平滑肌细胞增殖有抑制作用。这些结果提示血管损伤可致血管平滑肌细胞增殖；钙稳态失衡可能是血管损伤诱导血管平滑肌细胞增殖的细胞学机制之一。     

16肽－多聚赖氨酸携载β－LacZ基因向在体血管的导入与表达

１６肽－多聚赖氨酸携载β－ＬａｃＺ基因向在体血管的导入与表达北京医科大学心血管基础研究所赵民清，刘乃奎，周爱儒，汤健本实验室已报道ＢＱ１２３－多聚赖氨酸靶向地对血管平滑肌细胞转移外源基因，鉴于血管内皮细胞（ＥＣ）在心血管疾病中的重要作用，我们合成了内...     

纤维蛋白促血管平滑肌细胞增殖机制的研究

纤维蛋白促血管平滑肌细胞增殖机制的研究王雪青，刘乃奎，常英姿，唐朝枢（北京医科大学心血管基础研究所，北京１０００８３）纤维蛋白是一种有效的血管平滑肌生长刺激因素，然而其促平滑肌细胞（ＳＭＣ）增殖的机制尚不清楚。本研究发现，Ｆｂ可以有效地刺激ＳＭＣ内皮...