摘要
目的 探讨血红素氧合酶１（ＨＯ１） 和内源性一氧化碳（ＣＯ） 在哮喘发病机制中的作用及相互关系。方法 利用哮喘豚鼠模型及药物预防，用分光光度法检测豚鼠血一氧化碳血红蛋白（ＣＯＨｂ） 和血清及肺组织匀浆上清液ＨＯ１ 活性水平，放射免疫竞争抑制法检测血浆ｃＧＭＰ。结果 哮喘组全血ＣＯＨｂ （９．２ ±１．４） ％ ；ＨＯ１ 活性：血清（１１３．３±１７．７） ｎｍｏｌ／（Ｌ·ｈ）、肺组织（５５．５±５．６） ｎｍｏｌ／（ｍｇ·ｈ） ；血清ｃＧＭＰ（１．５９ ±０．３０） ｐｍｏｌ／ｍｇ，分别与地塞米松预防组和正常组比较差异有非常显著意义（ｔ＝ １１．５１ ～２２．４７，Ｐ＜ ０．０１）。地塞米松预防组与正常组比较，差异亦有非常显著意义（ 除ｃＧＭＰ外，Ｐ＜０．０１） 。血清与肺组织的ＨＯ１ 活性水平呈正相关，且分别与血ＣＯＨｂ 和ｃＧＭＰ 含量亦呈正相关（ｒ＝０．８６～０．９７， Ｐ＜０．０１） 。结论 哮喘时豚鼠体内ＨＯ１ 活性、内源性ＣＯ 和ｃＧＭＰ水平同时升高，三者在哮喘发病机制中具有重要的作用和必然的联系。
Objective To explore the mechanisms of heme oxygenase 1 (HO 1) and endogenous CO and the relationship between them in asthma Methods Guinea pig models of asthma were applied, some of them were treated with dexamethasone. Levels of HO 1 activity, COHb and cGMP in serum or lung tissue were determined by using spectrophotometry etc Results In acute asthmatic group, COHb in blood was (9 2±1 4)%, cGMP (1 59±0 30) pmol/mg and HO 1 activity was (113 2±17 7) nmol/(L·h) in serum and (55 5± 5 6) nmol/(mg·h) in lung These parameters significantly increased as compared with normal control group and dexamethasone treated group ( t =11 51～22 47, P <0 01) However, all the above parameters except for cGMP of dexamethasone treated group were higher than those of normal controls ( P <0 01) HO 1 activities in serum and lung tissue were positively correlated with each other or with the COHb and cGMP ( r =0 86～0 97, P <0 01) Conclusion In asthma, the increased HO 1 activity resulted in increase of endogenous CO that can enhance cGMP
出处
《中华儿科杂志》
CAS
CSCD
北大核心
1999年第9期562-564,共3页
Chinese Journal of Pediatrics
