【摘要】 本实验观察自由基发生系统(GSFR)对离体心脏和心肌细脂摄取~3H标记脂质体(DOPC/Chol/SA)的影响。结果发现GSFR使离体心脏脂质过氧化物MDA增加217.6％,同时,心脏摄取脂质俗的量增加55.9％,两者之间显著正相关(r=0.673,P<0.05)离体心肌细胞与GSFR孵育30分钟,细胞MDA含量增加4倍,而脂质体的摄取也增加48.9％。抗氧化剂维生索E能抑制GSFR的怍用,细胞MDA的含量和细胞摄取脂质体的量也明显减少。结果表明膜质脂过氧化促进心肌对脂质体的摄取,提示,膜脂质过氧化是缺氧、缺血及再灌法损伤时心肌摄取脂质体增加的可能机制之一。更多还原

【Abstract】 In the present study we observed the effects of generating system of free radicals (GSFR, FeSO4 and ascorbate) on uptake of liposomes (DOPC/Chol/ SA) labelled with 3H, by isolated rat heart and myocytes. The results showed that perfusion with GSFR increased products of lipid peroxidation, MDA, by 217.6% and uptake of liposomes by 55.9%. There was a positive correlation between the myocardial content of MDA and uptake of liposomes (r = 0.673, p<0.05) . After incubation with GSFR for 30min, the myocyte content of MDA was significantly increased 4 times and the uptake of liposomes was increased by 48.9%. The effects of GSFR on myocytes were inhibited by an-tioxidant, α-tocopherol,with the content of MDA and the uptake of liposomes. The results demonstrated that the lipid peroxidation of myocardial cell membrane prompted the myocardium uptake of liposomes, suggesting the membrane lipid peroxidation was one of the mechanisms of high uptake of liposomes in anoxia, ischemia and reperfusion.更多还原