摘要
目的观察无创性肢体缺血预适应(NLIP)对心脏缺血/再灌损伤后纤溶因子的影响,进一步探讨其对心脏的延迟保护作用。方法连续3d,每天1次,3个循环下肢无创性5min缺血,5min再灌建立NLIP模型。实验分3组:模型组(I/R);心脏缺血预适应组(CIP);NLIP组。再灌末取心肌组织,以四氮唑染色法测定心肌梗死面积(IS/AAR×100%)。取血,以发色底物法测定血浆中t-PA和PAI-1活性,以羟胺法测定血浆中SOD活性。结果与I/R组(44.5±8.1)%比较,CIP和NLIP能明显降低梗死面积(28.6%±9.5%和25.4%±8.7%,P<0.01);与I/R组t-PA(1.01±0.33)U·ml-1和PAI-1(27.11±0.63)AU·ml-1比较,CIP和NLIP均能明显对抗血t-PA活性的降低〔(1.98±0.46)和(1.89±0.44)U·ml-1,P<0.01〕和PAI-1活性的升高〔(25.42±0.56)和(22.01±0.45)AU·ml-1,P<0.01〕;与I/R组(300±49)NU·ml-1比较,CIP和NLIP均能明显提高再灌后SOD活性〔(366±72)和(388±67)NU·ml-1,P<0.05和P<0.01〕。结论NLIP对心肌缺血/再灌损伤具有保护作用,机制可能与其对纤溶系统的影响有关。
Aim To observe the effects of limb atraumatic ischemic preconditioning (NLIP) on the fibrolysis factors after myocardial ischemia-repeffusion (I/R) injury in rats. Methods RIP was performed in rats by a repeated three-cycle 5-min ischemia-repeffusion of hind limb everyday for three days. Three experimental groups were included:model, CIP and NLIP. The area at risk (AAR) and infarct area (IS) were determined using Trypan blue and triphenyl tetrazolium choride (TTC) staining respectively. The infarct size was defined as IS/AAR × 100%. To detect the activity of t- PA and PAI-1, chromogenic substrate method was adopted. SOD activity was detected with hydroxylamine method. Results Compared with I/R group (44.5 ±8.1 ) % , CIP and NLIP could decrease IS/AAR (28.6 ±9.5)% and (25.4 ±8.7)%,(P〈0.01). Compared with I/R group,CIP and NLIP could prevent the decrease of t-PA activity ( 1.98 ± 0. 46) and ( 1.89± 0.44) U · ml^-1,(P〈0.01) and the increase of PAI- 1 (25.42±0.56) and (22.01 ±0.45) AU · ml^-1, (P 〈 0.01 ). Meanwhile, CIP and NLIP could elevate SOD activity (366 ±72) and (388 ±67) NU · ml^-1, (P〈0.05 and P 〈0.01) compared with I/R group (300 ± 49) NU · ml^-1. Conclusions NLIP could protect against myocardial injury, and the mechanism might be related to fibrolysis system.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2008年第10期1344-1347,共4页
Chinese Pharmacological Bulletin
基金
天津市自然科学基金资助项目(No003608411)