肝硬化形成过程中血小板活性因子及其受体在门脉高压形成中的意义

目的　了解血小板活性因子 (PAF)及其受体在肝硬化门脉高压形成中的作用。方法　采用CCl4腹腔注射 8周 (2次 /周 )诱导大鼠肝硬化 ,利用ELISA、RT PCR及受体饱和结合实验检测PAF水平及其受体表达。结果　与对照组相比 ,肝硬化时肝内PAF、肝脏输出PAF及血清内PAF分别增高了 4 4 0 %、87 7%和 5 4 5 % (P <0 0 1,P <0 0 5 ,P <0 0 5 )。肝硬化大鼠肝内PAF受体mRNA表达及PAF结合高于对照组近 3倍 ,门脉压高于正常大鼠 2 31倍 (P <0 0 1)。结论　肝硬化时PAF系统上调节肝血流动力学和代谢异常是门脉高压形成的重要因素 ,肝内PAF释放入循环系统的增加是影响系统血流动力学异常改变的关键因子。

Increased production of hepatic platelet activating factor (PAF) and PAF receptors in CCl4-induced liver cirrhosis:its implications in chronic liver injury

Objective To explore the role of platelet activating factor(PAF) and its receptor in portal hypertension in liver cirrhosis. Methods A model of hepatic cirrhosis was replicated in rat by intraperitoneal injection of CCL 4 for 8 weeks. The blood and hepatic PAF and PAF receptors contents were assayed with ELISA, RT-PCR and saturation binding technique. Results Compared with control rats, cirrhotic rats had higher hepatic PAF levels, hepatic PAF output, and plasma PAF levels, which were increased by 44%, 87.7% and 54.5%(P<0.01, P<0.05, P<0.05), respectively. Hepatic PAF receptor mRNA levels and PAF binding were both nearly 3 fold greater in cirrhotic rats, which also exhibited higher baseline portal pressure (P<0.01). Conclusion The results suggest that the up-regulation of the PAF system contributes to hepatic hemodynamic and metabolic abnormalities in cirrhosis, and the increased release of PAF into the circulation also impacts systemic hemodynamics.