兔脑完全性缺血后再灌流时钙磷脂酶A_2和游离脂肪酸的变化

CHANGES OF CALCIUM, PHOSPHOLIPASE A_2 AND FREE FATTY ACIDS IN RABBIT BRAIN AFTER COMPLETE CEREBRAL ISCHEMIA

脑缺血后再灌流时发生的神经元损伤有多种致病因子参与。诸如:细胞内游离Ca^(2+)升高和组织钙总量增多,磷脂酶A_2(PLA_2)活化,细胞膜磷脂降解和游离脂肪酸(FFA)释放增加,曾先后见于文献报道。但是,如今存在的最大缺陷是对上述因子之间的相互关系尚无足够的认识。为了适当弥补上述缺陷和进一步认识它们在脑缺血后再灌流时的发病学意义。本研究采用“四血管式模型,在同一动物上同时检测了脑缺血后再灌流时上述因子的变化。

Using'four—vessel'model, we studied the changes of rabbit brain after complete cerebral ischemia and reperfusion (1) the total content of calcium in brain cortex tissue; (2) The activity of PLA_2 in BCM; (3) FFA in PMS.Rabbits were assigned randomly into three groups: (1) nonischemic (N=4); (2) ischemic (N=4); (3) ischemic with reperfus ion (N=12).Reperfusion animals were sacrificed at 30, 120 and 360 minof reperfusion.As compared with nonischemic controls, there was a significant increase in the total content of calcium at 30 and 360 minof reperfusion: the activity of PLA_2 in BCM increased significantly following ischemia and reperfusion,the FFA in PMS coincided with that of PLA_2, The results indicated that the changes of calcium, PLA_2 and FFA were closely related, and calcium—PLA_2—FFA might play an important role in neuronal damage in sequence following reperfusion.