期刊文献+

哮喘患者诱导痰中内皮素活性研究 被引量:1

The Effect of Endothelin in Induced Sputum from Patients with Asthma
原文传递
导出
摘要 目的 探讨内皮素 (ET)在哮喘发病过程中的作用及其与肺功能的相关性。方法 用高渗盐水诱痰法收集 2 5例轻、中度哮喘发作期患者 ,2 6例哮喘缓解期患者及 30名健康者的痰标本 ,用放射免疫法测定其中ET的浓度。结果 ⑴FEV1/FVC发作组最低 ,缓解组次之 ,正常组最高 ,各组比较差异均有显著性 (均P <0 0 1)。⑵发作组和缓解组诱导痰中炎症细胞数均明显高于正常组 (均P <0 0 1)。⑶发作组诱导痰中ET浓度明显高于缓解组和正常组 (均P <0 0 1)。⑷发作组诱导痰中ET浓度与FEV1/FVC和氧分压均呈负相关 (r分别为 - 0 76 2、- 0 878) ,而与巨噬细胞数呈正相关 (r =- 0 6 53)。结论 哮喘发作期和缓解期患者气道腔内均存在慢性非特异性炎症。ET可能参与了哮喘的病理进展过程 ,并在哮喘的气道炎症和气道重塑中起了重要作用 ;诱导痰中ET的浓度可较好地反映气道腔局部ET浓度的变化。 Objective To investigate the role of endothelin(ET) in the pathogenesis of asthma and analyze the relationship between level of endothelin in induced sputum and pulmonary function:forced expiratory volume/forced vital capacity(FEV 1/FVc).Methods Induced sputum was obtained by inhaling 5% saline.Endothelin level in induced sputum obtained from 25 patients with mild or moederate attacking asthma(Group Ⅰ),26 patients with stable asthma(Group Ⅱ) and 30 healthy controls(Group Ⅲ) were measured by radioimmunoassay.Results ⑴FEV 1/FVC in Group Ⅱ was higher than those in Group Ⅰ(P<0.01),and lower than those in Group Ⅲ(P<0.01),respectively.⑵The number of all inflammatory cells and macrophages in induced sputum from both the Group Ⅰ and Group Ⅱ were higher than those from the Group Ⅲ(P<0.01),respectively.⑶The level of ET in induced sputum from Group Ⅰ was higher than those from both Group Ⅱ and Group Ⅲ(P<0.01),respectively.⑷The level of ET in induced sputum from Group Ⅰ was negatively correlated with FEV 1/FVC and oxygen partial pressure(PaO 2),and positively correlated with the number of macrophages.Conclusions There is non-specific chronic airway inflammation in patients with asthma.Endothelin may be involved in the pathological process of asthma,especially in the airway inflammation and its remodeling.The level of ET in induced sputum can reflect the level of ET in airway.
作者 朱凯勋
出处 《中国医师杂志》 CAS 2001年第4期266-268,共3页 Journal of Chinese Physician
关键词 哮喘 内皮素 Asthma Sputum Endothelin
  • 相关文献

参考文献4

二级参考文献3

共引文献2019

同被引文献22

引证文献1

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部