肝硬变门脉高压休克再灌注胃粘膜损伤的实验研究  

STUDY ON GASTRIC MUCOSAL INJURY INDUCED BY SHOCK REPERFUSION IN PORTAL HYPERTENSION RATS WITH CIRRHOSIS

作　　者：徐泽宽[1] 张保康[1] 

机构地区：[1]南京医科大学第一附属医院普外科

出　　处：《中国普外基础与临床杂志》1998年第5期267-269,共3页Chinese Journal of Bases and Clinics In General Surgery

摘　　要：本实验应用电子自旋共振（ＥＳＲ）技术及自旋捕捉剂ＰＢＮ直接测定肝硬变门脉高压（ＰＨＴ）大鼠胃粘膜在休克再灌注前后及应用超氧化物歧化酶（ＳＯＤ）、丹参（ＲＳＭ）治疗后氧自由基（ＯＦＲ）的动态变化，同时检测胃粘膜中ＳＯＤ活性，并观察同期胃粘膜的光镜、电镜病理改变。结果：ＰＨＴ胃粘膜在休克再灌注过程中有大量ＯＦＲ产生，粘膜损伤的严重程度与ＯＦＲ含量及ＳＯＤ活性密切相关；ＰＨＴ胃粘膜更易受休克再灌注时ＯＦＲ的损伤，早期应用抗氧化剂ＳＯＤ及ＲＳＭ，可通过不同机理减轻胃粘膜再灌注损伤。Electron spin resonance (ESR) spectroscopy and spin trapping agent PBN were applied to measure directly the changes of oxygen free redicals (OFR) in gastric mucosa of rats with portal hypertension (PHT) injured by shock reperfusion, and treated with superoxide dismutase (SOD), radix salviae miltiorrhizae (RSM), with concomitant monitoring activity of SOD and pathology of gastric mucosa. Results showed that the amount of OFR increased markedly in gastric mucosa of PHT rats during the shock reperfusion. The pathological changes were in accordance with alteration of the amount of OFR and the activity of SOD. Gastric mucosa in PHT was more susceptible to shock reperfusion insult than normal controls. The anti oxidant SOD, RSM used at early stage exerted mild gastric mucosal insult through different mechanisms.

关 键 词：肝硬变 休克 再灌注 门静脉高压 胃粘膜损伤 

分 类 号：R657.340.6[医药卫生—外科学] R573.02[医药卫生—临床医学]