高压氧对急性一氧化碳中毒大鼠脑一氧化氮及一氧化氮合酶的影响

Effect of hyperbaric oxygenation on brain nitric oxide and nitric oxide synthase of carbon monoxide poisoning rats

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.