门脉高压症猪脾组织中内皮素受体及诱导型一氧化氮合酶mRNA表达的意义

探讨胆汁性肝硬化门脉高压症猪脾组织中内皮素受体(ETR)及诱导型一氧化氮合酶(iNOS)mRNA的表达及其对内脏血流动力学的影响.采用原位杂交方法检测实验组(n=10)和对照组(n=5)猪脾组织冰冻切片中ETR(ETAR、ETBR)及iNOS mRNA的表达.同时监测猪的门脉血流量(Qpv)、门静脉压(PPv)及平均动脉压(MAP).结果,实验组ETAR mRNA表达水平与对照组无显著差异(P＞0.05),而ETBR及iNOS mRNA表达水平显著高于对照组(P＜0.01),其中ETAR mRNA表达主要位于血管平滑肌细胞中;ETBR mRNA主要位于脾窦内皮细胞;iNOS mR-NA主要在血管平滑肌细胞、巨噬细胞和内皮细胞中.ETAR mRNA的表达与Qpv、Ppv无明显相关(P=0.11或P=0.08);ETBR与iNOS mRNA的表达水平分别与Qpv、PPv呈正相关(P＜0.05或P＜0.01);而分别与MAP呈负相关(P＜0.05或P＜0.01).研究表明ETBR及iNOS mRNA的表达可能在门脉高压症和内脏高血流动力学中起重要作用.

Significance of Endothelin Receptors and Inducible Nitric Oxide Synthase mRNA Expression in Splenic Tissue of Porcine with Portal Hypertension

The gene expression of endothelin receptors (ET A R, ET B R) and inducible nitric oxide synthase (iNOS) in splenic tissue of porcine biliary cirrhosis with portal hypertension and the effects of these changes on splanchnic hyperdynamics of portal hypertension (PHT) were investigated. Fifty porcine were divided into experimental group receiving common bile duct ligation ( n =10) and sham operated group ( n =5). ET A R, ET B R and iNOS mRNA expression was detected by in situ hybridization in frozen sections of splenic tissue. Porcine Qpv, Ppv and MAP were monitored simultaneously. The results showed that there was no significant differences in ET A R mRNA expression between the two groups ( P >0 05). However, ET B R and iNOS mRNA expression levels in the experimental group were significantly higher than in sham operated group ( P <0 01). ET A R mRNA was expressed predominantly in vascular smooth muscle cells,ET B R mRNA in splenic sinusoidial cells,iNOS mRNA in vascular smooth muscle cells, macrophages and endothelial cells,respectively. No significant correlation was found between ET A R mRNA expression and Ppv or Qpv( P =0 11 or P =0 08). ET B R and iNOS mRNA expression levels were positively related to Qpv and Ppv( P <0 05 or P <0 01), but negatively to MAP( P <0 05 or P <0 01). It suggests that ET B R and iNOS mRNA expression may play an important role in the pathogenesis of portal hypertension and splanchnic hyperdynamics.