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作 者:刘华[1] 杜婧[1] 陈更业[1] 王玉巧[1] 张龙[1]
机构地区:[1]宁夏回族自治区人民医院呼吸内科,银川750021
出 处:《宁夏医科大学学报》2009年第3期332-334,共3页Journal of Ningxia Medical University
摘 要:目的探讨尾加压素Ⅱ(U-II)在慢性阻塞性肺疾病(COPD)发病中的变化及意义。方法采用放射免疫法测定34例COPD患者和10例正常健康人血浆及诱导痰中U-II含量,并常规进行肺功能检测和诱导痰细胞计数和分类。结果COPD组患者肺功能下降,FEV1占预计值百分数和FEV1/FVC比值均显著低于对照组(P<0.01);血气分析示COPD组PaO2亦显著低于对照组(P<0.01);COPD组诱导痰中细胞总数、中性粒细胞数、巨噬细胞数均显著高于对照组(P均<0.05)。COPD患者和健康对照组血浆U-II含量差异无统计学意义(P>0.05),而COPD患者诱导痰U-II含量较对照组升高(P<0.05),COPDⅢ、Ⅳ级患者诱导痰U-Ⅱ含量[130.01(121.03,149.88)μg/L]显著高于I、Ⅱ级患者[101.99(97.84,114.00)μg/L](P<0.05)。COPD患者和对照组诱导痰U-II含量分别为血浆含量的81倍和64倍,诱导痰和血浆U-II水平无相关(r=0.171,P>0.05)。诱导痰U-II水平与诱导痰细胞总数和中性粒细胞数呈正相关(分别r=0.449,r=0.428,P均<0.01),与FEV1占预计值百分数和血PO2呈负相关(分别r=-0.490,r=-0.521,P均<0.05)。结论COPD时气道U-II分泌增加,U-II可能以旁分泌/自分泌的方式参与慢性阻塞性肺疾病的发病。Objective To investigate the roles of urotensin H ( U - Ⅱ ) in chronic obstructive pulmonary disease (COPD). Methods Plasma and induced sputum were obtained from thirty four patients with stable COPD and ten healthy volunteers. The levels of U - Ⅱ in plasma and induced sputum were measured by RIA kit. Lung function was performed routinely. Induced sputum cells were counted with hemacytometer and differentiated with Wright - Giemsa stain. Results The levels of U - Ⅱ in induced sputum were 81and 64 folds higher than those of plasma U - Ⅱ in COPD patients and healthy controls (P 〈 0.01 ). The levels of U - Ⅱ in plasma were unrelated to those of induced sputum( r = 0. 171, P 〉 0.05 ). No difference was noted between COPD and healthy controls in the plasma U -Ⅱ levels( P 〉 0.05 ). Sputum U - Ⅱ levels from COPD patients were 16% higher than those of healthy controls. Induced sputum U - Ⅱ levels of COPD patients had a trend of increase as lung function deteriorated. Raised sputum total cell and neutrophil counts correlated strongly with the levels of U - Ⅱ in induced sputum( r =0.449, r =0.428, P all 〈0.01 ). The levels of U - Ⅱ in induced sputum correlated negatively with FEV1% predicted and PO2 ( r = - 0.490 r = - 0. 521, P all 〈 0.05. Conclusion U - Ⅱ may act locally or via paracrine or autocrine way, play a role in the mechanism of the airway inflammation and airway remodeling in COPD.
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