内源性一氧化碳与低氧性肺动脉高压关系的临床研究

被引:3
作者
刘雅
孙培宗
欧阳松云
王东昕
机构
[1] 郑州大学第一医院呼吸内科,郑州大学第一医院呼吸内科,郑州大学第一医院呼吸内科,河南省平顶山市煤业集团总医院呼吸内科郑州,郑州,郑州
关键词
高血压,肺性; 一氧化碳; 内皮素1;
D O I
暂无
中图分类号
R543.2 [肺动、静脉疾病];
学科分类号
1002 ; 100201 ;
摘要
目的 探讨慢性肺心病 (简称肺心病 )患者血浆内源性一氧化碳 (CO)水平及内皮素 1(ET 1) /CO与低氧性肺动脉高压 (HPH)的关系。方法 采用Chalmers介绍的血红蛋白结合及联二亚硫酸盐还原法检测 33例肺心病患者急性加重期和缓解期血浆内源性CO水平 ,同步测定血浆ET 1水平、动脉血氧分压 (PaO2 )及右室射血前期时间与肺动脉血流加速时间的比值 (RVPEP/AT) ,并进行相关分析。 30名性别和年龄相匹配的健康人作为对照组。结果 肺心病组急性加重期和缓解期患者血浆内源性CO、ET 1和ET 1/CO水平为 (1.34± 0 .18)mg/L、(1.0 7± 0 .14 )mg/L ;(82± 15 )ng/L、(5 7±10 )ng/L ;6 1± 6、5 3± 5 ,与正常对照组 [(0 .5 5± 0 .12 )mg/L、(2 7± 9)ng/L、4 8± 7]比较 (P均 <0 .0 0 1和 <0 .0 5 ) ;急性加重期与缓解期比较 (P均 <0 .0 0 1和 0 .0 5 )。肺心病组急性加重期和缓解期血浆内源性CO水平均与PaO2 呈负相关 (r =- 0 .733、- 0 .6 72 ,P均 <0 .0 1) ,与RVPEP/AT呈正相关 (r =0 6 2 0、0 .5 5 7,P均 <0 .0 1) ;血浆ET 1/CO均与RVPEP/AT呈正相关 (r =0 .5 0 1、0 .4 85 ,P <0 .0 1和0 0 5 )。结论 肺心病患者血浆内源性CO水平升高可能参与了HPH的病理生理过程并发挥重要的代偿作用 ,ET 1和CO比值失衡可
引用
收藏
页码:34 / 37
页数:4
相关论文
共 8 条
[1]  
Carbon monoxide-induced vasorelaxation and the underlying mechanisms. Wang R,Wang Z,Wu L. British Journal of Pharmacology . 1997
[2]  
Simple, sensitive measurement of carbon monoxide in plasma. Chalmers AH. Clinical Chemistry . 1991
[3]  
Heme oxygenase-1: function, regulation, and implication of a novel stress-inducible protein in oxidant-induced lung injury. Choi AM,Alam J. Am J Respir Cell Mol Biol . 1996
[4]  
Hemodynamic force induce the expression of heme oxygenase in cultured vascular smooth muscle cells. Wagner CT,Durante W,Christodoulides N,et al. The Journal of Clinical Investigation . 1997
[5]  
Increased levels of exhaled carbon monoxide in bronchiectasis: a new marker of oxidative stress. Horvath I,Loukides S,Wodehouse T,et al. Thorax . 1998
[6]  
Increased carbon monoxide in exhaled air of subjects with upper respiratory tract infections. Yamaya M,Sekizawa K,Ishizuka S,et al. American Journal of Respiratory and Critical Care Medicine . 1998
[7]  
The heme oxygenase system: a regulator of second messenger gases. Maines MD. Annual Review of Pharmacology and Toxicology . 1997
[8]  
Endothelial cell expression of vasoconstrictors and growth factors is regulated by smooth muscle cell-derived carbon monoxide. Morita T,Kourembanas S. The Journal of Clinical Investigation . 1995