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硝苯地平在对慢性阻塞性肺疾病患者的肺动脉高压进行短期而非长期治疗期间可降低肺动脉压和血管张力。

Nifedipine reduces pulmonary pressure and vascular tone during short- but not long-term treatment of pulmonary hypertension in patients with chronic obstructive pulmonary disease.

作者信息

Agostoni P, Doria E, Galli C, Tamborini G, Guazzi M D

机构信息

Istituto di Cardiologia, University of Milan, Italy.

出版信息

Am Rev Respir Dis. 1989 Jan;139(1):120-5. doi: 10.1164/ajrccm/139.1.120.

Abstract

We evaluated in patients suffering from COPD-related pulmonary hypertension whether nifedipine therapy lowers acutely and chronically pulmonary vascular pressure and resistance and whether pulmonary transmural pressure may be further lowered by the combined use of nifedipine and oxygen. Changes of the pulmonary vascular tone were determined on the pulmonary driving pressure/flow curve, which was generated by upright exercise. Fifteen patients with COPD and mean pulmonary pressure greater than or equal to 20 mm Hg were studied at control (Week 0) and after 1 wk of nifedipine treatment (180 mg daily, Week 1). It was possible to pursue the same nifedipine daily dosage for 2 months in 10 patients, who were re-evaluated after 8 wk of treatment and after nifedipine withdrawal the following week. At Week 1, mean pulmonary transmural pressure was reduced (32.8 +/- 4.1 versus 27.3 +/- 2.8 mm Hg, mean +/- SE, p less than 0.05) via active pulmonary vasodilation because the pulmonary driving pressure/flow curve was shifted right and downward. Both mean transmural pulmonary pressure lowering effect and active pulmonary vasodilatation regressed during long-term nifedipine treatment. Oxygen reduced pulmonary transmural pressure (32.8 +/- 4.1 versus 28.6 +/- 2.9 mm Hg, p less than 0.05, Week 0); however, this effect always disappeared during nifedipine treatment. We conclude that nifedipine should not be used as long-term treatment for COPD-related pulmonary hypertension and that nifedipine inhibits the oxygen capability to reduce pulmonary pressure.

摘要

我们评估了硝苯地平治疗对慢性阻塞性肺疾病(COPD)相关肺动脉高压患者急性和慢性肺血管压力及阻力的降低作用,以及硝苯地平和氧气联合使用是否可进一步降低肺跨壁压。通过直立运动生成肺驱动压力/流量曲线,以此确定肺血管张力的变化。研究了15例平均肺动脉压大于或等于20 mmHg的COPD患者,在对照期(第0周)和硝苯地平治疗1周后(每日180 mg,第1周)进行观察。10例患者能够维持相同的硝苯地平每日剂量2个月,在治疗8周后及随后一周停用硝苯地平后再次进行评估。在第1周,通过有效的肺血管舒张,平均肺跨壁压降低(32.8±4.1对27.3±2.8 mmHg,均值±标准误,p<0.05),因为肺驱动压力/流量曲线向右下移位。在长期硝苯地平治疗期间,平均跨壁肺压降低作用和有效的肺血管舒张均消退。氧气可降低肺跨壁压(32.8±4.1对28.6±2.9 mmHg,p<0.05,第0周);然而,在硝苯地平治疗期间这种作用总是消失。我们得出结论,硝苯地平不应作为COPD相关肺动脉高压的长期治疗药物,且硝苯地平会抑制氧气降低肺压的能力。

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