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硝苯地平对慢性阻塞性肺疾病患者肺气体交换的有害作用。

Deleterious effect of nifedipine on pulmonary gas exchange in chronic obstructive pulmonary disease.

作者信息

Melot C, Hallemans R, Naeije R, Mols P, Lejeune P

出版信息

Am Rev Respir Dis. 1984 Oct;130(4):612-6. doi: 10.1164/arrd.1984.130.4.612.

Abstract

Nifedipine was given, 20 mg sublingually, to 6 patients with pulmonary hypertension secondary to advanced chronic obstructive pulmonary disease, and its effects on hemodynamics, blood gases, lung mechanics, and the distribution of ventilation-perfusion ratios (VA/Q) were investigated. Systemic vasodilation was obtained, with a reduction in mean systemic arterial pressure and in systemic vascular resistance by 16 and 36%, respectively. Cardiac index increased by 29%. Pulmonary vascular resistance decreased by 28%, without changes in pulmonary arterial mean pressure. Arterial PO2 decreased from 52 +/- 4 to 47 +/- 3 mmHg (p less than 0.001). A deterioration in VA/Q matching could be demonstrated, with a redistribution of blood flow into the lungs by a diversion of 20% of total blood flow from units with normal VA/Q, between 0.23 to 3.0, to hypoxic units with low VA/Q between 0.19 to 0.009. These changes might be explained by a partial inhibition of hypoxic pulmonary vasoconstriction.

摘要

对6例晚期慢性阻塞性肺疾病继发肺动脉高压患者舌下含服20毫克硝苯地平,并研究其对血流动力学、血气、肺力学以及通气-灌注比(VA/Q)分布的影响。获得了全身血管舒张,平均全身动脉压和全身血管阻力分别降低了16%和36%。心脏指数增加了29%。肺血管阻力降低了28%,肺动脉平均压无变化。动脉血氧分压从52±4降至47±3毫米汞柱(p<0.001)。可以证明VA/Q匹配恶化,20%的总血流量从VA/Q正常(0.23至3.0)的单位分流到VA/Q低(0.19至0.009)的缺氧单位,导致肺内血流重新分布。这些变化可能是由于缺氧性肺血管收缩受到部分抑制所致。

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