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急性重症哮喘中肾素-血管紧张素系统的研究

Investigations on the renin-angiotensin system in acute severe asthma.

作者信息

Ramsay S G, Dagg K D, McKay I C, Lipworth B J, McSharry C, Thomson N C

机构信息

Dept of Respiratory Medicine, Western Infirmary, Glasgow, Scotland, UK.

出版信息

Eur Respir J. 1997 Dec;10(12):2766-71. doi: 10.1183/09031936.97.10122766.

Abstract

The renin-angiotensin system is activated in acute severe asthma. The precise mechanism of activation is at present unknown, but may involve, beta2-agonists, catecholamines or proteases released in airway inflammation. This study aims to identify potential factors involved in the activation of the renin-angiotensin system in acute asthma. Forty asthmatics with severe exacerbations of asthma, assessed by measurement of peak expiratory flow rate (mean (SD) 35 (18)% predicted), oxygen saturation (94 (4)%) and pulse rate (108 (16) beats x min(-1)) were recruited. Nineteen (48%) asthmatics had elevated plasma angiotensin II levels (median (interquartile range) 10.9 (4.3-23.5) pg x mL(-1) (normal range 3-12 pg x mL(-1))) and 10 (25%) had elevated plasma renin concentration (22.0 (10.0-50.0) microU x mL(-1) (normal range 9-50 microU x mL(-1))). Plasma renin and angiotensin II correlated strongly, implying renin-dependent angiotensin II formation. No correlation was found between plasma salbutamol, adrenaline, nor-adrenaline, endothelin-1, histamine, eosinophilic cationic protein, serum angio-tensin-converting enzyme (ACE) activity, total immunoglobulin E (IgE), urea and electrolytes, indicators of the severity of the attack, atopic status, blood pressure and renin or angiotensin II levels. We conclude that although a subpopulation of asthmatics appear to have raised renin and angiotensin II during attacks of acute, severe asthma, the mechanism of activation of the renin-angiotensin system remains unclear.

摘要

肾素-血管紧张素系统在急性重症哮喘中被激活。目前激活的确切机制尚不清楚,但可能涉及β2受体激动剂、儿茶酚胺或气道炎症中释放的蛋白酶。本研究旨在确定急性哮喘中参与肾素-血管紧张素系统激活的潜在因素。招募了40名哮喘严重加重的患者,通过测量呼气峰值流速(平均(标准差)为预测值的35(18)%)、血氧饱和度(94(4)%)和脉搏率(108(16)次/分钟)进行评估。19名(48%)患者的血浆血管紧张素II水平升高(中位数(四分位间距)为10.9(4.3 - 23.5)pg/mL(正常范围3 - 12 pg/mL)),10名(25%)患者的血浆肾素浓度升高(22.0(10.0 - 50.0)微单位/mL(正常范围9 - 50微单位/mL))。血浆肾素和血管紧张素II密切相关,提示血管紧张素II的形成依赖肾素。在血浆沙丁胺醇、肾上腺素、去甲肾上腺素、内皮素-1、组胺、嗜酸性阳离子蛋白、血清血管紧张素转换酶(ACE)活性、总免疫球蛋白E(IgE)、尿素和电解质、发作严重程度指标、特应性状态、血压与肾素或血管紧张素II水平之间未发现相关性。我们得出结论,尽管在急性重症哮喘发作期间,一部分哮喘患者似乎肾素和血管紧张素II升高,但肾素-血管紧张素系统的激活机制仍不清楚。

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