门静脉高压症病人肝内血管内皮细胞凋亡的研究

A study on intrahepatic vascular endothelial cell apoptosis in patients with portal hypertension

目的 研究门静脉高压症病人肝组织内血管及肝窦壁内皮细胞的凋亡及其对肝微循环的影响。方法 对 37例门静脉高压症病人、10例正常人肝组织 ,用TUNEL法检测血管内皮细胞及肝窦壁内皮细胞凋亡 ,免疫组化法检测Bax和Bcl 2基因的蛋白表达。结果 肝硬化门静脉高压症病人 ,门管区血管内膜破坏、断裂 ,内皮细胞脱落。管腔内血栓形成。血管壁和肝窦壁内皮细胞TUNEL 阳性细胞数为 (2 9 2 9± 4 15 ) % ,与对照组仅 (0 5± 0 2 ) % ,有显著性差异 (P <0 0 0 1) ;门管区血管内皮细胞和肝窦壁内皮细胞Bax和Bcl 2强阳性表达率分别为 (33 5 1± 5 6 9) %和 (2 4 6 4± 5 87) % ,对照组均为阴性 (P <0 0 0 1)。结论 肝硬化门静脉高压症病人门管区内皮细胞和肝窦壁内皮细胞凋亡和坏死明显增加 ,内皮细胞的凋亡和坏死激活凝血系统 ,促使血栓形成 ,从而破坏了肝脏微循环。

Objective To investigate the intrahepatic vascular and hepatic sinusoidal endothelial cell (SEC) apoptosis and its influence on hepatic microcirculation in patients with portal hypertension. Methods The apoptosis of VECs and hepatic SECs was examined with TUNEL. The expression of Bax and Bcl 2 protein was analyzed by immunohistochemical technique in 37 cases of portal hypertension and 10 normal individuals. Results Vascular endothelial membrane of portal hypertension show destruction, cleavage and dropout accompanying with thrombosis in the vascular cavity. TUNEL positive cells of VECs and hepatic SECs were (29 29±4 15)% in patients with portal hypertension but only (0 5±0 2)% in normal controls. There was significant difference between the two groups (P<0 001). The Bax and Bcl 2 immunostaining-positive cells were (33 51±5 69)% and (24 64±5 87)% in the patients and normal controls, respectively. Bax was markedly higher than Bcl 2 (P<0 001). Conclusions Apoptosis and necrosis of VECs and SECs occur in portal area in patients with portal hypertension, which activates the blood coagulation system, promotes thrombosis and destroys hepatic microcirculation.