新生儿缺氧缺血性脑病内源性一氧化碳的变化  

Changes of endogenous carbon monoxide in newborn infants with hypoxic ischemic encephalopathy

作　　者：史源[1] 李华强[1] 潘凤[1] 潘捷[1] 覃世文[1] 沈际皋[1] 

机构地区：[1]第三军医大学附属大坪医院野战外科研究所儿科,重庆400042

出　　处：《中华儿科杂志》1999年第8期499-500,共2页Chinese Journal of Pediatrics

摘　　要：目的　探讨内源性一氧化碳（ＣＯ） 在新生儿缺氧缺血性脑病（ＨＩＥ） 中的作用。方法　对２８ 例（ 轻度组１３ 例，中度组１０ 例，重度组５ 例）ＨＩＥ 新生儿血浆ＣＯ 水平进行测定。结果　２８ 例ＨＩＥ新生儿血浆ＣＯ水平为（２．１５±０．２０） ｍｇＬ，高于正常对照组的（１．４９ ±０．２０） ｍｇＬ，（ Ｐ＜ ０．０５）。血浆ＣＯ 水平的高低与病情严重程度密切相关，重度患儿ＣＯ 水平为（２．８８±０．９７） ｍｇＬ，较轻、中度者为高［（１．７０±０．８７） ｍｇＬ、（１．９７±１．０１） ｍｇＬ］，（Ｐ均＜ ０．０５）。结论　ＣＯ可能作为一种内源性介质参与新生儿ＨＩＥ的发病过程。Objective To study the role of endogenous carbon monoxide (CO) in neonatal hypoxic ischemic encephalopathy (HIE) Methods The plasma CO levels were detected in newborn infants with HIE Results The plasma CO levels in 28 newborn infants with HIE were significantlty higher than those in the normal controls [(2 15±0 20) mg/L vs (1 49±0 20) mg/L ( P <0 05)] Moreover, the plasma CO levels were related to the severity of neonatal HIE The newborn infants with severe HIE had significantly higher CO levels [(2 88±0 97) mg/L] than those with the mild [(1 70±0 87) mg/L] and moderate HIE [(1 97±1 01) mg/L, P <0 05 respectively] Conclusion The present study suggests that CO as an endogenous mediator might take part in the pathogenesis of neonatal HIE

关 键 词：婴儿 新生 一氧化碳 脑缺氧 脑缺血 

分 类 号：R722.120.2[医药卫生—儿科]