Effect of Angiotensin Converting Enzyme Inhibition on Airway Conductance during Hypocapnic Hyperventilation in Normal Subjects

Pulmonary pharmacology Pub Date : 1995-02-01 DOI:10.1006/pulp.1995.1007

J.P. Jamison, P.J. Glover

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引用次数: 2

Abstract

Summary: In nine normal subjects, specific airway conductance was measured by whole body plethysmography before and immediately after hypocapnic hyperventilation. This procedure, forced expiratory manoeuvres and arterial blood pressure measurements were carried out before and 4 h after placebo and the angiotensin converting enzyme inhibitor, enalapril, in a double-blind, randomized study design.

Bronchoconstriction to hypocapnic hyperventilation was shown by a reduction in specific airway conductance on all occasions (P<0.001).

A reduction in mean blood pressure was obtained after enalapril compared to placebo (P<0.05).

No significant change attributable to enalapril was observed in any lung function measurement either at rest or immediately after hypocapnic hyperventilation, despite an expected enhancement of endogenous angiotensin converting enzyme activity by alkalosis.

Inhibition of angiotensin converting enzyme revealed no effect of the endogenous activity of this enzyme on airway calibre either at rest or during the bronchoconstrictor response to hypocapnic hyperventilation.

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血管紧张素转换酶抑制对正常人低碳酸血症过度通气时气道传导的影响

摘要:在9名正常受试者中，在低碳酸血症过度通气之前和之后立即用全身容积描记仪测量特定气道导度。采用双盲随机研究设计，在安慰剂和血管紧张素转换酶抑制剂依那普利治疗前和治疗后4小时分别进行用力呼气操作和动脉血压测量。低碳酸血症过度通气导致的支气管收缩在所有情况下都表现为特定气道导度的降低(P<0.001)。与安慰剂相比，依那普利可降低平均血压(P<0.05)。尽管碱中毒预期会增强内源性血管紧张素转换酶的活性，但在静息或低碳酸血症过度通气后的任何肺功能测量中，依那普利均未观察到可归因于依那普利的显著变化。抑制血管紧张素转换酶显示内源性活性的这种酶对气道口径没有影响，无论是在休息或在支气管收缩反应低碳酸血症过度通气。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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Pulmonary pharmacology

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