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前列环素与门静脉高压症高动力循环的关系
作者姓名:Wu ZY  Chen XS  Cao H
作者单位:200127,上海第二医科大学附属仁济医院普外科
摘    要:目的 探讨前列环素 (PGI2 )和一氧化氮 (NO)在门静脉高压症高血流动力循环中的作用。 方法  66只雄性SD大鼠随机分成 :肝内型门静脉高压症组 (IHPH组 )、肝前型门静脉高压症组 (PHPH组 )和假手术组 (SO组 )。模型制备 1周后再随机分为 3个亚组 ,即对照组、一氧化氮合酶抑制剂L NNA组、消炎痛组。用药 1周后测定股动脉血浆 6 酮 前列腺素F1α(6 keto PGF1α)和NO2 - /NO3- 浓度 ,应用同位素微球技术行血流动力学研究 ,并对NO、PGI2 水平与血流动力学参数行Pearson相关分析。 结果  (1 )在基础状态下 ,血浆 6 keto PGF1α浓度 ,IHPH鼠 (1 1 2 3 85± 1 53 64)pg/ml]和PHPH鼠 (891 88± 83 1 1 )pg/ml]均显著地高于SO鼠 (72 5 53± 1 0 5 54)pg/ml] ,P <0 0 5 ;血浆NO2 - /NO3- 浓度 ,IHPH鼠 (73 34± 4 31 ) μmol/L]和PHPH鼠 (75 2 1± 6 89) μmol/L]均显著高于SO鼠(58 79± 8 47) μmol/L] ,P <0 0 5。 (2 )与对照组比较 ,L NNA与消炎痛均显著地降低IHPH与PHPH 2组鼠血浆 6 keto PGF1α和NO2 - /NO3- 的浓度 ,P <0 0 5 ;降低IHPH、PHPH 2组鼠的心脏指数 (CI)、门静脉压力 (FPP)和门静脉血流量 (PVI) ,P <0 0 5 ;显著地增高这 2组鼠的平均动脉压 (MAP)、总外周血管阻力 (TPR)和内脏血

关 键 词:前列环素  门静脉高压症  高血流动力循环  一氧化氮合酶抑制剂  测定  6-酮-前列腺素F1α
修稿时间:2002年7月26日

The effect of PGI2 on formation and development of hyperdynamic circulatory state in portal hypertensive rats
Wu ZY,Chen XS,Cao H.The effect of PGI2 on formation and development of hyperdynamic circulatory state in portal hypertensive rats[J].Chinese Journal of Surgery,2003,41(7):537-540.
Authors:Wu Zhi-yong  Chen Xue-song  Cao Hui
Institution:Department of General Surgery, Renji Hospital, Shanghai Second Medical University, Shanghai 200127, China.
Abstract:OBJECTIVE: To investigate the effects of prostacyclin (PGI(2)) and nitric oxide (NO) in the development of hyperdynamic circulatory state on chronic portal hypertensive rats. METHODS: Sixty-six male SD rats were divided into three groups, namely intrahepatic portal hypertension (IHPH) by injection of CCl(4), prehepatic portal hypertension (PHPH) by partial stenosis of the portal vein for 2 weeks and sham-operated controls (SO). Animals in each group were divided further into 3 subgroups and received N(omega)-nitro-L-arginine (L-NNA), indomethacin and saline (as control), respectively. Splanchnic and systemic hemodynamics was measured using radioactive microsphere techniques. The NO concentration in serum was determined by nitrates-intrites which were measured using a colorumetric method, and concentration of PGI(2) was determined using specific radioimmunoassay for its stable hydrolytic product, 6-keto-PGF(1alpha). RESULTS: The concentrations of plasma 6-keto-PGF(1alpha) and serum nitrates + nitrites in IHPH rats (1 123.85 +/- 153.64; 73.34 +/- 4.31) and in PHPH rats (891.88 +/- 83.11; 75.21 +/- 6.89) were significantly higher than those of SO rats (725.53 +/- 105.54;58.79 +/- 8.47). L-NNA and indomethacin could decrease the concentrations of plasma 6-keto-PGF(1alpha) and serum nitrates + nitrites in IHPH and PHPH rats (P < 0.05). At the same time, CI, FPP and PVI were lowered while MAP, TPR and SVR were increased (P < 0.05). After deduction of NO action, there were no significant correlation between plasma PGI(2) level and hemodynamic parameters such as CI, TPR, PVI and SVR. However, after deduction of PGI(2) action, NO was still correlated highly with those hemodynamic parameters. CONCLUSION: It is NO rether then PGI(2) that is a mediator in the formation and development of hyperdynamic circulatory state in chronic portal hypertensive rats.
Keywords:Hypertension  portal  Epoprostenol  Nitric oxide
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