摘要
探讨氧自由基 (OFR)在失血性休克再灌注损伤中的作用及牛磺酸的保护效应。健康家兔 2 4只随机分为 3组(n =8) :对照组、单纯休克组、牛磺酸治疗组 ;采用失血性休克再灌注损伤模型。连续观察休克前 ,休克 1.5h ,再灌注 1h、2h、3h时血浆超氧化物歧化酶 (SOD)活性、丙二醛 (MDA)含量、乳酸脱氢酶 (LDH)活性的动态变化 ;并测定再灌注 3h时心、肺组织MDA含量和SOD活性。结果显示 ,1)单纯休克组再灌注各时限MDA含量、LDH活性显著升高 ;SOD活性显著下降。 2 )再灌注 3h时心、肺组织MDA含量显著升高 ;SOD活性显著下降。 3)牛磺酸 (40mg·kg-1,iv)可减轻再灌注各时限上述指标的变化 (均P <0 .0 1)。提示OFR介导了休克再灌注损伤 ,牛磺酸对休克再灌注损伤的保护作用可能与减少OFR的生成和促进自由基的清除有关。
The paper investigates the role of oxygen free radical(OFR) in hemorrhagic shock/reperfusion injury and protective effect of taurine on it. Twenty four rabbits were divided randomly into 3 groups(n=8): control group,shock group,taurine group. The model of hemorrhagic shock/reperfusion was used. The activities of superoxide dismutase(SOD),lactate dehydrogenase(LDH)and the content of malondialdehyde(MDA)in plasma were observed before shock and shock 1.5 hours,reperfusion 1 hour,2 hours and reperfusion 3 hours. Meanwhile,the activities of SOD and the contents of MDA in lung and heart were measured at 3 hours reperfusion. Result show:1)The activities LDH and the contents of MDA increased significantly,but the activities of SOD decreased markedly in shock group during shock/reperfusion. 2)The contents of MDA in the lung and heart increased significantly,but the activity of SOD decreased markedly at 3 hours reperfusion. 3) Taurine(40 mg·kg\+\{-1\},iv) could attenuate all the changes mentioned above at total time points of reperfusion. These results suggested that OFR may be involved in the pathogenesis of shock/reperfusion,the protective effect of taurine on reperfusion injury might be related to decreasing the generation of OFR and strengthening scavenging of OFR.
出处
《石河子大学学报(自然科学版)》
CAS
2002年第4期276-278,共3页
Journal of Shihezi University(Natural Science)