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目的:研究一氧化氮(NO)在缺血性脑损伤中的作用。方法:沙土鼠前脑缺血性脑损伤模型,分组、分剂量进行。结果:小剂量N~G-硝基-L-精氨酸(LNNA)能明显减轻缺血性损伤后脑含水量。脑损伤后一氧化氮合酶(NOS)活力明显升高,LNNA能抑制NOS活力,抑制程度与剂量相关。缺血性损伤后海马神经元严重缺失。中、小剂量LNNA能减轻海马神经元缺失,而大剂量LNNA能加重神经元缺失。结论:脑缺血后NOS活性明显增加,加重缺血性脑损伤。适当降低脑组织NOS活性能明显减轻脑水肿和海马细胞坏死。提示NO对脑损伤毒性作用和保护作用与NO浓度相关。
Objective: To study the role of nitric oxide (NO) in ischemic brain injury. Methods: The model of gerbil forebrain ischemia brain injury was divided into groups and divided doses. Results: Low-dose N-G-nitro-L-arginine (LNNA) significantly reduced brain water content after ischemic injury. After brain injury, the activity of nitric oxide synthase (NOS) was significantly increased. LNNA could inhibit the activity of NOS. The degree of inhibition was dose-dependent. Hippocampal neurons are severely deficient after ischemic injury. Medium and low doses of LNNA can reduce the loss of hippocampal neurons, and high doses of LNNA can aggravate neuronal loss. Conclusion: The activity of NOS after cerebral ischemia is obviously increased, which aggravates the ischemic brain injury. Appropriate to reduce brain tissue NOS activity can significantly reduce cerebral edema and hippocampal cell necrosis. It is suggested that the toxic effect of NO on brain injury and its protective effect are related to NO concentration.