感冒后咳嗽敏感性及气道神经源性炎症改变

被引:63
作者
陈如冲
刘春丽
罗炜
姚卫民
钟淑卿
赖克方
钟南山
机构
[1] 广州医学院第一附属医院广州呼吸疾病研究所
关键词
咳嗽; 感冒后咳嗽; 咳嗽敏感性; 神经源性炎症; 发病机制;
D O I
暂无
中图分类号
R56 [呼吸系及胸部疾病];
学科分类号
摘要
目的观察感冒后咳嗽患者(cough post infectious,CPI)的咳嗽敏感性以及气道分泌物神经肽变化,探讨其可能的发病机制。方法以2005年1~6月于广州呼吸疾病研究所慢性咳嗽专科门诊诊断10例CPI患者(CPI组)及10名正常志愿者(正常对照组)为研究对象,通过辣椒素咳嗽激发试验测定气道咳嗽敏感性;观察诱导痰细胞总数以及细胞分类比例;测定痰上清液P物质(SP)、神经肽A(NKA)、神经肽B(NKB)及降钙素基因相关肽(CGRP);检测诱导痰细胞SP、NKA及SP受体(NK-1)的表达,并进行分析比较。结果CPI组咳嗽阈值lgC5为1.16±0.61,明显低于正常对照组(2.64±0.28)(P<0.001)。CPI组诱导痰细胞总数(WBC)及细胞分类比例与正常对照组差异均无显著性意义。CPI组诱导痰上清液SP质量浓度为(516.3±494.2)ng/L,显著高于正常对照组[(141.7±34.5)ng/L,P<0.05];CGRP质量浓度为(141.2±80.8)ng/L,显著高于正常对照组[(74.3±38.2)ng/L,P<0.05];而2组间NKA、NKB的质量浓度差异均无显著性意义。CPI组痰细胞SP、NK-1蛋白的表达分别为1.86±0.81和1.20±0.75,显著高于正常对照组的(0.65±0.44和0.27±0.24)(P<0.01);而2组间NKA蛋白表达差异无显著性意义。结论CPI患者的咳嗽敏感性增高,并伴随气道神经源性炎症,提示其与CPI发病相关。
引用
收藏
页码:674 / 676+679 +679
页数:4
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