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出 处:《中华理疗杂志》1999年第4期224-226,共3页Chinese Journal of Physical Therapy
摘 要:目的观察急性一氧化碳(CO)中毒大鼠脑组织中一氧化氮(NO)、一氧化氮合酶(NOS)活性的变化及高压氧(HBO)对其影响。方法建立实验性大鼠CO中毒模型。采用改良的Gries法和分光光度法分别测定CO染毒及HBO或常压氧治疗后大脑和小脑中NO、NOS活性。结果CO中毒后小脑NO明显增至(1.36±0.34)μmol/gprot,NOS活性受抑制,为(3.76±0.32)nmol/min·gprot;HBO治疗使NO、NOS均恢复正常水平,分别为(1.07±0.37)μmol/gprot,(5.33±0.93)nmol/min·gprot。CO中毒后大脑NO降低到(0.47±0.14)μmol/gprot,NOS活性受抑制,为(1.88±0.41)nmol/min·gprot,HBO治疗使NO增高至(0.73±0.24)μmol/gprot,NOS活性恢复正常(4.88±1.22)nmol/min·gprot。结论急性CO中毒使大脑及小脑NO、NOS活性均发生改变,此种改变可能参与CO造成的脑损伤。HBO治疗对NO、NOS变化有极为有益的调节作用。Objective The purpose of this study was to evaluate the nitric oxide(NO) level and nitric oxide synthase(NOS) activity in the carbon monoxide(CO) poisoning rat brain after hyperbaric oxygenation(HBO) therapy.Methods First,the rat CO poisoning models were set up experimentally.The NO level and NOS activity in cerebral and cerebellum were respectively measu red by Griess method and spectrophotometry before and after HBO therapy.Results Generally,at post-CO poisoning,the NO level of cerebellum was obviously enhanced(1.36±0.34)μmol/gprot,the NOS activity was inhibited (3.76± 0.32)nmol/min·gprot. Through the HBO treatment,the NO level and NOS activity were all returned to normal baseline,they were (1.07±0.37)μmol/gprot and (5.33±0.93)nmol/min·gprot respectively.While the NO level was reduced (0.47±0.14)μmol/gprot and the NOS activity was also inhibited (1.88±0.41)nmol/min·gprot in cerebral after CO poisoning.After HBO treatment,the NO level was raised (0.73± 0.24)μmol/gprot and NOS activity was returned to normal (4.88±1.22)nmol/min·gprot.Conclusion It shows that acute CO poisoning may influence the change of NO and NOS activity in the brain.This change is related to neurologic damdage.HBO can regulate the NO and NOS activity and is an effective therapy for acute CO poisoning.
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