摘要
目的 :研究血小板激活因子拮抗剂SRI6 3 - 44 1对大鼠缺血再灌注损伤心肌的保护作用。方法 :将实验大鼠分成 3组 ,对照组未行缺血及药物治疗 ,再灌注组及SRI6 3- 44 1治疗组结扎大鼠左冠状动脉前降支 (LAD)缺血 30min后 ,行再灌注 10h ,其中治疗组结扎前 1min给予SRI6 3 - 44 1(1mg/kg) ,观察大鼠再灌注心律失常 ,再灌注区心肌组织中丙二醛浓度、超氧化物歧化酶活性的变化。结果 :SRI6 3- 44 1能明显降低再灌注时室性心律失常的严重程度 ,使缺血 30min再灌注 10h大鼠的心肌梗塞面积从 (2 1 6± 3 1) %降至 (12 7± 2 5 ) % ,心肌组织中脂质过氧化最终产物丙二醛 (MDA)含量下降 ,超氧化物歧化酶 (SOD)活性升高。结论 :SRI6 3 - 44 1用于大鼠心肌缺血再灌注可减少心肌损伤 ,揭示PAF为心肌再灌注损伤的重要介质 ,而PAF拮抗剂有可能用于心肌缺血再灌注损伤的治疗。
Objective:TO study the effects of PAF antagonist SRI63-441 on ischemia-reperfusion(I/R)injury of the myocardium.Methods:Rat models of I/R were established with coronary occlusion and reperfusion of the left anterior descending artery (LAD). The rats were randomiy divided into 3groups:control group,reperfusion group and PAF goup. LAD of the rats in control group was not occluded.The rats in PAF group and reperfusion group were given SRI63-441(lmg/kg)and BSA-phosphoric-acid buffer solution by intravenous injection one minute before the occlusion of LAD,respectively.The change of arrhythmia,myocardial infarct size(MIS),superoside dismutase(SOD)activity and malondialdehyde(MDA)level were measured.Results:The MIS,severity of arrhythmia and levels of MDA decreased,while the activities of SOD increased.Conclusion:PAF might be an important mediator involved in myocardial reperfusion injury.PAF antagonist may be useful in the treatment of myocardial I/R injury.
出处
《西南国防医药》
CAS
2003年第1期25-28,共4页
Medical Journal of National Defending Forces in Southwest China
