肺泡低氧是引起肺血管收缩的原因,若肺血管收缩持续存在,将导致肺动脉肌化和持续性肺动脉高压。动物和人的研究表明,通过持续抑制低氧性肺血管收缩,由慢性低氧所引起的上述病理改变能逆转。然而,对许多患者不能提供或不允许持续用氧,用药物抑制上述反应可能非常有益。作者发现硝苯吡啶能显著逆转低氧性肺血管收缩,在休息和运动时能降低肺血管阻力及肺动脉压。本文6例病情稳定的低氧性肺动脉高压者(5例为COPD,1例严重脊柱后凸畸形),无左心衰史,近期无呼吸功能衰竭。以研究硝苯吡啶对肺动脉压,肺血管阻力,动脉氧含量及氧释放等方面的作用。 Alveolar hypoxia is the cause of pulmonary vasoconstriction, if pulmonary vasoconstriction persists, will lead to pulmonary arterialization and persistent pulmonary hypertension. Animal and human studies have shown that the above pathological changes caused by chronic hypoxia can be reversed by sustained inhibition of hypoxic pulmonary vasoconstriction. However, for many patients, it is not possible to provide or disallow continuous use of oxygen and it may be very beneficial to use drugs to inhibit such reactions. The authors found that nifedipine significantly reversed hypoxic pulmonary vasoconstriction and decreased pulmonary vascular resistance and pulmonary arterial pressure during rest and exercise. 6 cases of stable hypoxic pulmonary hypertension (5 cases of COPD, 1 case of severe kyphosis), no history of left heart failure, no recent respiratory failure. To study the effects of nifedipine on pulmonary arterial pressure, pulmonary vascular resistance, arterial oxygen content and oxygen release.