氯喹,SOD防治脑缺血再灌注损伤的实验研究

探讨氯喹、超氧化物歧化酶（ＳＯＤ）防治脑缺血再灌注损伤的效果。用４血管阻断法造成大鼠全脑缺血，３０ｍｉｎ后再恢复双侧颈总动脉血流３０ｍｉｎ，此时大鼠脑组织磷脂酶Ａ（ＰＬＡ）活性和内皮素（ＥＴ）、过氧化脂质（ＬＰＯ）含量显著增高，而ＳＯＤ活性和维生素Ｅ（ＶｉｔＥ）含量明显降低，大脑皮层神经细胞和血脑屏障明显损害。预防用氯喹或ＳＯＤ治疗，部分抑制了ＬＰＯ、ＥＴ含量的增高和ＳＯＤ活性下降，明显减轻脑神经细胞和血脑屏障损伤程度；但对ＶｉｔＥ含量都无明显影响。氯喹、ＳＯＤ对缺血再灌注脑损伤有一定的防治作用。

Chloroquine or SOD protecting rat , s brain from postischemic reperfusion injury

Protective effects of chloroquine or superoxide dismatase(SOD) on brain of Wistar rats with cerebral postischemic reperfusion was studied. The complete cerebral ischemic models were made by 4 vessel occlusion in awake Wistar rats. By 30 min reperfusion after 30 min complete cerebral ischemia in rats, phospholipase A 2 (PLA 2 ) activities and values of endothelins(ET) and lipid peroxidation(LPO) increased(all P<0.05), but SOD activities and vitamin E(Vit E) Valaues decreased(all P<0.05) in brain tissues. At the same time, Blood brain barriers and cortex neuronal ultrastructures were damaged severely. By pretreatment with chloroquine or SOD, the increases of PLA 2 activities and levels of ET and LPO, the decreases of SOD activities in brain tissue were all inhibited significantly(all P<0.05). At the same time, the cerebral postischemic reperfusion injury was reduced. There were no significant effects on values of Vit E in brain tissue. Effects of chloroquine can partly inhibit PLA 2 activities in brain tissue. Chloroquine and SOD have protective effects on brain in Wistar rat with cerebral postischemic reperfusion.