摘要
目的:探讨肝窦内皮在内皮素-1(ET-1)诱导大鼠门脉高压以及丹酚酸B干预过程中的变化。方法:将20只SD大鼠随机分为4组,均采用门静脉穿刺灌流。在灌流缓冲液5min后,预防对照组予灌流ET-1缓冲液,中药预防组予丹酚酸B+ET-1灌流液,治疗对照组予ET-1液灌流及缓冲液,中药治疗组予ET-1及丹酚酸B灌流液。分别观察4组大鼠各时段门脉灌流压后处死取材,通过形态学方法,观察ET-1诱导大鼠门脉压升高及丹酚酸B干预的过程中肝窦内皮窗孔的变化。结果:在ET-1诱导大鼠门脉灌流压升高过程中,肝窦内皮细胞窗孔体积缩小,数量减少;用含丹酚酸B的缓冲液灌流后,大鼠门静脉灌流压较对照组低,肝窦内皮细胞窗孔体积变大,数量增多。结论:肝窦内皮在ET-1诱导大鼠门脉压升高的过程中可能起着重要的作用;活血化瘀药丹参的有效成分丹酚酸B能有效预防或改善由ET-1诱导的肝窦内皮细胞失窗孔及门脉压的升高。
Objective: To study the morphologic change of hepatic sinusoid endothelium during ET-1 induced portal hypertension in rats and its intervention by Salvianolie-acid B. Methods: Twenty SD rats were randomly divided into four groups, then in situ liver perfusion was performed to detect the portal pressure of rats. We performed an in situ perfusion of rat livers with 10-9 mol/L ET-I and 10-5 mol/L Salvianolic-acid B; after 5-minute perfusion, morphologic methods were used to study the changes of hepatic sinusoid endothelium during ET-1 induced portal hypertension and intervention by Salvianolic-acid B. Results: Intraportal infusJ.on of 10-9 mol/L endothelin-1 significantly elevated portal venous pressure. The reduction in the number of fenestrae of sinusoidal endothelial cells was obvious during ET-1 induced portal hypertension; SA-B significantly down-regulated the high portal vein pressure induced by extragenous ET-1, the number of fenestrae of sinusoidal endothelial cells was much more than in con- trol group. Conclusion: Hepatic sinusoid endothelium change is the vital cause of portal hypertension induced by ET-1.
出处
《上海中医药大学学报》
CAS
2007年第6期54-57,共4页
Academic Journal of Shanghai University of Traditional Chinese Medicine
基金
上海市重点学科建设基金资助项目(T0301)
上海市教委科研基金资助项目(01C02)