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目的探讨门静脉压力升高和门静脉体循环分流与前列环素(PGI_2)水平升高的关系。方法 36只雄性 SD 大鼠随机分为四组:肝前型门静脉高压(PHPH)8只和肝内型门静脉高压(IHPH)9只,端侧门静脉下腔静脉分流(PCS)8只及正常对照组(假手术)(SO)11只。模型制备后2周:(1)测游离门静脉压(FPP);(2)应用核素微球技术研究全身及内脏血流动力学;(3)用放射免疫法测股动脉血浆6-酮-前列腺素 F_(1α)(6-keto-PGF_(1α))浓度。结果 (1)IHPH 和 PHPH 组的 FPP 高于 SO 鼠(P<0.05),而 PCS 鼠低于 SO鼠(P<0.05)。PCS 和 PHPH 鼠心指数(CI)大于 SO 鼠(P<0.05)。IHPH、PHPH 及 PCS 鼠中 PVI 均高于 SO 鼠(P<0.05),且以 PCS 鼠为著。(2)血浆6-keto-PGF_(1α)浓度前三组大于 SO 组(P<0.05),且 PH-PH 和 IHPH 鼠均大于 PCS 鼠(P<0.05)。血浆6-keto-PGF_(1α)浓度与 FPP 值之间呈正相关(r=0.67,P<0.01)。结论门静脉高压时 PGI_2升高主要是门静脉压力升高的结果,而门静脉体循环分流和肝功能减退起次要作用。本研究结果不支持 PGI_2参与门静脉高压高血流动力状态的发生。
Objective To investigate the relationship between the elevation of portal vein pressure and the circulation of portal vein circulation and the elevation of prostacyclin (PGI_2). Methods Thirty-six male Sprague-Dawley rats were randomly divided into four groups: 8 of hepatic portal hypertrophy (PHPH), 9 of intrahepatic portal hypertension (IHPH), 8 of inferior vena cava venous shunt (PCS) and 8 normal controls Group (sham) (SO) 11 only. 2 weeks after model preparation: (1) FPP; (2) systemic and visceral hemodynamics were studied using radionuclide microscopy; (3) radioimmunoassay was used to measure 6-keto- Prostaglandin F_ (1α) (6-keto-PGF_ (1α)). Results (1) The FPP in IHPH and PHPH groups was higher than that in SO rats (P <0.05), while that in PCS rats was lower than that in SO rats (P <0.05). The heart index (CI) of PCS and PHPH was greater than that of SO mice (P <0.05). The PVI in IHPH, PHPH and PCS rats were higher than that in SO rats (P <0.05), and that in PCS rats. (2) Plasma 6-keto-PGF_ (1α) concentrations were higher in the first three groups than in the SO group (P <0.05), and were higher in the PH-PH and IHPH mice than in the PCS mice (P <0.05). The plasma concentration of 6-keto-PGF_ (1α) was positively correlated with FPP (r = 0.67, P <0.01). Conclusions The elevation of PGI_2 in portal hypertension is mainly caused by the increase of portal pressure, while the circulation of portal vein and hepatic dysfunction play a secondary role. The results of this study do not support the PGI_2 involved in the occurrence of portal hypertension in high blood flow dynamic state.