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肝硬化患者血浆刺激内皮产生一氧化氮的实验研究 被引量:4

Plasma from patients with cirrhosis increases nitric oxide release from vacular endothelial cells in vitro
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摘要 目的 研究肝硬化患者血浆能否刺激血管内皮细胞产生一氧化氮。方法 分别用正常人血浆和肝硬化患者血浆刺激人脐静脉血管内皮细胞,以硝酸还原酶法测定细胞培养上清NO浓度,逆转录-聚合酶链反应(RT-PCR)测定血管内皮细胞NO(eNOs)mRNA水平。结果肝硬化患者血浆组NO浓度显著高于正常人血浆组(P≤0.01);门静脉高压症患者血浆处理组eNOS mR-NA水平较正常人血浆组增高,且有时间依赖性,正常人血浆处理样品的各个时间点其RNA水平没有明显差异。结论 肝硬化患者血浆本身可刺激血管内皮细胞产生NO。 Objective To study weather plasma from patients with cirrhosis could stimulate vacu-lar en3othelial cells to increase the release of nitric oxide (NO) in vitro. Methods Human umbilical vascular endothelial cells (HUVEC) were stimulated by plasma from patients with cirrhosis and from normal subjects respectively. Concentrations of NO secreted were detected by the means of nitrate reductase, and eNOs mRNA level by reverse transcription-polymerase chain reaction. Results Concentration of NO was significantly higher with exposure to plasma from patients with cirrhosis than that of normal controls (P≤0.01).The expression of eNOS mRNA was higher with exposure to plasma from patients with cirrhosis than that of normal controls in a time-dependent fashion. There was no significant difference in the eNOS mRNA expression in the normal controls at different time points. Conclusion Plasma from patients with cirrhosis itself could increase the release of NO.
出处 《中华实验外科杂志》 CAS CSCD 北大核心 2004年第9期1060-1061,共2页 Chinese Journal of Experimental Surgery
关键词 肝硬化患者 人血浆 正常人 刺激 血管内皮细胞 一氧化氮 NO浓度 MRNA水平 时间依赖性 细胞培养 <Keyword>tric oxide Nitric oxide synthase Plasma Cirrhosis Endothelial cell
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参考文献4

  • 1Buga GM,Gold ME,Fukuto JM.Shear stress-induced release of nitric oxide from endothelial cells grown on beads.Hypertension,1991,17:187-193.
  • 2Rubanyi GM,Romero JC,Vanhoutte PM.Flow-induced release of endothelium-derived relaxing factor.Am J Physiol,1986,250:H1145-H1149.
  • 3Wiest R,Shah V,Sessa WC.Nitric oxide overproduction by eNOS precedes hyperdynamic splanchnic circulation in portal hypertensive rats.Am J Physiol,1999,276:43-51.
  • 4Iwakiri Y,Tsai MH,McCabe TJ.Phosphorylation of eNOS initiates excessive NO production in early phases of portal hypertension.Am J Physiol Heart Circ Physiol,2002,282:H2084-H2090.

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