局灶性鼠脑缺血时一氧化氮及一氧化氮合酶抑制剂的作用机制

Investigation of effects of nitric oxide and nitric oxide synthase inhibitors administrated during the focal cerebral ischemia reperfusion in rats

目的研究一氧化氮在鼠脑局灶性脑缺血再灌注损伤中的作用。方法用线栓法建立大鼠大脑中动脉区缺血再灌注模型，分别用选择性和非选择性诱导型一氧化氮合酶抑制剂对鼠脑局灶性缺血再灌注过程中脑组织一氧化氮的变化规律及可能作用进行探讨。结果非选择性一氧化氮合酶抑制剂（Ｌ－ＮＡＭＥ）可加重局灶性脑缺血性损害，而选择性诱导型一氧化氮合酶抑制剂（ａｍｉｎｏｇｕａｎｉｄｉｎｅ，ＡＧ）具有明确的脑保护作用。结论不同类型的一氧化氮合酶所产生的一氧化氮在脑局灶性缺血性损害中具有不同的作用。

Objective To study the role of nitric oxide that might have double edged pathophysiological effects during the cerebral ischemic reperfusional injury. Method The rat models of middle cerebral artery (MCA) focal cerebral ischemia reperfusion were established with the suture method in the study. The nonselective NOS inhibitor and selective NOS inhibitor were used for investigating the effects of nitric oxide (NO) changes in the focal ischemic brain tissues and their respective roles during the cerebral ischemia reperfusion. Results This study showed that the nonselective NOS inhibitor L NAME (15 mg/kg) intraperitoneally administrated aggravated the ischemic brain injury,but selective NOS inhibitor aminoguanidine (150mg/kg) intraperitoneally given had a definite, protective effect on the brains. Conclusion The results implied that the NO from different cells and isoforms of NOS had unlike roles in focal cerebral ischemic reperfusional injury.