金属硫蛋白参与皮瓣缺血预处理的延迟保护作用

METALLOTHION CAN REINFORTH THE DELAYED PROTECTION THROUGH PRECONDITION OF FLAP ISCHEMIA

目的 :金属硫蛋白 (MT)参与皮瓣缺血预处理 (PC)延迟保护作用(DP)的可能性。 方法 :在猪背阔肌岛状皮瓣PC和培养肌细胞缺氧PC的模型上 ,检测PC后即刻 ,12hr和 2 4hrMT含量变化 ,观察PC后 2 4hr对再次长时间缺血 再灌注或缺氧 复氧损伤的保护作用 (皮瓣坏死范围 ,细胞存活率 ,LDH释放和细胞MDA含量 )以及用PD0 980 59抑制PC后MT含量增高对PC和DP的影响。 结果 :MT含量在PC后 12hr (肌细胞 )和 2 4hr (肌细胞和皮瓣组织 )显著增高 ,与未PC的皮瓣组织或肌细胞遭受I R或A R的损伤相比较 ,PC后 2 4hr其皮瓣坏死范围缩小 ,血浆LDH活性升高程度减轻 ,肌细胞成活率增高 ,细胞MDA含量和LDH释放均降低。用PD0 980 59抑制MT生成增多时 ,则消除了PC后的DP作用 ,上述皮瓣损伤指标接近单纯I R组或A R组 (P >0 0 5 )。 结论 :1 PC后 2 4hr皮瓣或肌细胞对再次I R或A R的损伤有保护作用 ;2 MT参与了皮瓣或肌细胞PC后的DP作用。

We try to study if matallothion participates the process of protecting the flaps which has been preconditioned with ischemia Methods:On the models of island flaps of musculus latissmus dosi of pigs and cultured myocyte,both have been preconditioned respectively by ischemia and anoxia,we have detected the change of the content of MT instantly,12 hours later and 24 hours later then we have observed the protection from damage of again disposition of ischemia/reperfus of anoxia/reoxygenation(from the area of flap necrosis,servival rate of cells,the quantity of LDH discharged and the content of MDA in the cells) and what would be with the delayed protection if the MT was inhibited by PD 098059 Results:The content of MT,12 hours later in myocyte and 24 hours in myocyte and flap tissue from being conditioned,increased obviously Compared with non conditioned flap tissue or myocyte,the necrosis areas of the preconditioned flaps were smaller,the activity increases of the hematoplasmas LDH were lower,the servival rate of myocyte is higher,the content of cell MDA and the quantity of discharged LDH is less When the generation of MT was inhibited by PD 098059,we observed that the DP of PC was removed and the above quotas of damage of the flaps were close to those of the group of simple I/R or A/R(P>0 05)which was preconditioned 24 hours ago Conclusion:①The flaps and myocytes which are preconditioned 24 hours ago have protection from again damage of I/R or A/R ②MT is involved in DP in the preconditionde flaps or myocytes