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机构地区:[1]中国医科大学附属第一医院急诊科,辽宁沈阳110042
出 处:《中风与神经疾病杂志》2001年第1期19-21,共3页Journal of Apoplexy and Nervous Diseases
摘 要:目的 研究高压氧(HBO)对急性一氧化碳(CO)中毒大鼠小脑组织中一氧化氮(NO)、一氧化氮合酶(NOS)活性的影响,探讨NO、NOS与急性CO中毒脑损伤的关系及HBO对NO、NOS的作用机制。方法 实验用Wistar大鼠80只,随机分为5组:正常对照组(C),CO染毒组(CO),CO染毒+HBO 1次治疗组(HBO1),CO染毒+HBO 3次治疗组(HBO3),CO染毒+常压氧(NBO) 1次治疗组(NBO1)。每组处理结束后取其小脑组织。采用改良的Griess法、分光光度法分别测定小脑组织中NO、NOS活性。结果 小脑中CO中毒后NO明显增高(P<0.05),HBO治疗后明显降低(P<0.05),而NBO治疗无此种改变;CO中毒后NOS活性明显降低(P<0.01),HBO治疗、NBO治疗后NOS活性均明显增高(P<0.01)。结论 (1)急性CO中毒后小脑组织中NOS活性受抑制,HBO治疗、NBO治疗均使NOS活性显著恢复。(2)急性CO中毒后NO在小脑中明显增高,HBO治疗可恢复小脑中NO含量,而NBO无此作用。Objective To study levels of nitric oxide (NO ) and nitric oxide synthase (NOS) in the rat cerebellum after exposure to carbon monox ide with or without HBO therapy. Methods Eighty male Wistar rats were randomly divided into 5 groups: control group,CO exposurewi without treatment,CO exposure with 1 HBO treatment,CO exposure with 3 HBO treatments,CO exposure with one normobaric oxygen (NBO) treatment NO levels were measured by Griess' method, and NOS activity was measured respectively by spectrophotometry. NO, NOS levels were com pared among the 5 groups. Results In the rat cerebellum , the level of NO increased and the level of NOS decreased after CO exposure. The level of NO decreased after HBO therapy, but not after NBO therapy. NBO and HBO therapy resulted in a return of NOS levels to baseline. Conclusions Activity of NOS was inhibited in the cerebell um after (CO) exposure. Both HBO and NBO therapies restored NOS activity. The production of NO increased in the cerebellum after CO exposure and only HBO (not NBO) restored NO production at the site. The demonstrated changes in levels of NO and NOS may play an important role in the central nerve system damage resulting from CO poisoning. NBO protected brain tissue after CO exposure in certain extent.
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