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L-精氨酸对大鼠高肺血流所致肺血管结构重建及内源性硫化氢的影响
引用本文:石琳,杜军保,齐建光,魏冰,唐朝枢. L-精氨酸对大鼠高肺血流所致肺血管结构重建及内源性硫化氢的影响[J]. 基础医学与临床, 2004, 24(2): 184-187
作者姓名:石琳  杜军保  齐建光  魏冰  唐朝枢
作者单位:北京大学,第一医院,儿科,北京,100034;北京大学,心血管研究所,北京,100034
基金项目:国家重点基础性研究项目 (G2 0 0 0 0 5 6 90 5 ),北京市自然科学基金 (70 330 4 7),北京大学生物医学跨学科研究项目,北京大学 985重大心血管疾病研究项目
摘    要:探讨L 精氨酸 (L Arg)对高肺血流量所致大鼠肺血管结构重建和内源性硫化氢的影响及其机制。 2 1只SD大鼠随机分为对照组 (n =7) ,分流组 (n =7) ,分流 +L 精氨酸组 (n =7)。对后两组大鼠行腹主动脉、下腔静脉分流术。对分流 +L 精氨酸组大鼠每天灌胃L Arg 1g kg。 1 1周后观察肺动脉平均压 (mPAP)和右心室肥厚的改变。并且在光学显微镜和电子显微镜下观测肺血管结构的变化。测定血浆硫化氢含量和肺组织硫化氢产出率。结果表明 ,分流组大鼠mPAP、右心室 /体重 (RV BW)及右心室 /左心室 +室间隔 [RV (LV +S) ]比值明显高于对照组 (P <0 0 1 ) ,光镜下肺小血管肌化程度明显增强 ,电镜下 ,肺中、小肌型动脉内皮细胞增生、肥厚 ,平滑肌细胞由收缩表型向合成表型转化。分流组大鼠的血浆H2 S含量及肺组织CSE活性 (肺组织H2 S产出率 )明显低于对照组 (P <0 0 1 ) ,肺动脉平均压与血浆H2 S浓度呈负相关。同时L Arg缓解了肺动脉结构重建的形成 ,同时提高了内源性硫化氢水平 ,这可能是L Arg缓解高肺血流量所致肺动脉高压形成的机制之一。

关 键 词:精氨酸  硫化氢  肺动脉高压  左向右分流  大鼠
文章编号:1001-6325(2004)02-0184-04
修稿时间:2003-06-06

Effects of L-arginine on pathologic structure and endogenous hydrogen sulfide pathway in rats with pulmonary hypertension induced by high pulmonary blood flow
SHI Lin,DU Jun bao,QI Jian guang,WEI Bing,et al.. Effects of L-arginine on pathologic structure and endogenous hydrogen sulfide pathway in rats with pulmonary hypertension induced by high pulmonary blood flow[J]. Basic Medical Sciences and Clinics, 2004, 24(2): 184-187
Authors:SHI Lin  DU Jun bao  QI Jian guang  WEI Bing  et al.
Abstract:To explore the therapeutic effect of L arginine on pathologic structure and endogenous hydrogen sulfide pathway in rats with pulmonary hypertension induced by high pulmonary blood flow. Twenty one SD rats were randomly divided into shunting group (n=7) ,shunting with L arginine group(n=7)and concrol group(n=7).L arginine was orally given in the rats of shunting with L arginine group. An 11 week aortocaval shunting was produced in shunting and shunting with L arginine rats, pulmonary artery mean pressure (mPAP) and the ratio of right ventricular mass to boby weight (RV/BW)and right ventricular mass to left ventricular plus septal mass[RV/(LV+S)] were evaluated. Pulmonary vascular micro and ultra structure were also examined. Meanwhile the concentration of plasma hydrogen sulfide (H 2 S) was measured by spectrophoteries. The activity of CSE in lung tissues was measured by H 2 S production according to chemical analysis. After 11 weeks of aortocaval shunting,we found that pulmonary artery mean pressure was significantly increased. Muscularization of small pulmonary vessels and relative medial thickness of pulmonary arteries were obviously increased in shunting rats as compared with the controls. Ultrastructure of intrapulmonary arteries changed obviously in shunting rats. Meanwhile, plasma H 2 S concentration decreased and the activity of CSE (according to H 2 S production )in lung tissues decreased in shunting rats. However, mPAP and RV/BW,RV/LV+S significantly decreased in rats in shunting with L arginine group as compared with shunt rats( P <0.05).L arginine ameliorated pulmonary vascular structural remodeling in shunting rats in association with a changed endogenous hydrogen sulfide pathway. The result showed that L arginine may play an role in the regulation of development of high pulmonary blood flow induced pulmonary hypertension and pulmonary vascular structural re constructed by changing endogenous H 2 S pathway.
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