Fisher J, Mack R J, Likier H M, Schiff A N, Borer J S
Chest. 1987 Sep;92(3):400-5. doi: 10.1378/chest.92.3.400.
We studied (via acute vasodilator testing with nifedipine) 27 patients with pulmonary arterial hypertension (PAH) (11 primary, 16 secondary PAH, [including six patients with Raynaud's phenomenon]) in order to identify predictors of hemodynamic response and specifically to assess whether patients with Raynaud's phenomenon and pulmonary hypertension were more likely to respond to nifedipine. Nifedipine decreased resting mean pulmonary artery (PA) pressure and pulmonary vascular resistance (PVR) in patients with Raynaud's phenomenon (delta PA - 6.8 +/- 10.5 mm Hg; delta PAD - PCW gradient - 9.3 +/- 4.7 mm Hg; delta PVR - 255 +/- 201 dynes.s.cm-5, all p less than .05) versus (delta PA 0.3 +/- 4.0 mm Hg; delta PAD - PCW gradient 0.4 +/- 5.0 mm Hg; delta PVR - 58 +/- 132 dynes.sec.cm-5, all NS), in the patients without Raynaud syndrome. These data suggest that patients with both primary and secondary PAH may benefit from nifedipine therapy, but that patients with Raynaud's phenomenon may respond particularly well, perhaps because of vasodilator-reversible pulmonary vasoconstriction. An alternative hypothesis is that prior chronic vasodilator therapy in the majority of our patients with Raynaud's phenomenon preserved pulmonary vasoreactivity.
我们（通过使用硝苯地平进行急性血管扩张试验）研究了27例肺动脉高压（PAH）患者（11例原发性，16例继发性PAH，[包括6例雷诺现象患者]），以确定血流动力学反应的预测因素，并特别评估患有雷诺现象和肺动脉高压的患者是否更有可能对硝苯地平产生反应。与无雷诺综合征的患者相比（ΔPA 0.3±4.0 mmHg；Δ肺动脉舒张压-肺毛细血管楔压梯度0.4±5.0 mmHg；Δ肺血管阻力-58±132达因·秒·厘米⁻⁵，均无统计学意义），硝苯地平降低了患有雷诺现象患者的静息平均肺动脉（PA）压和肺血管阻力（PVR）（ΔPA -6.8±10.5 mmHg；Δ肺动脉舒张压-肺毛细血管楔压梯度-9.3±4.7 mmHg；Δ肺血管阻力-255±201达因·秒·厘米⁻⁵，均p<0.05）。这些数据表明，原发性和继发性PAH患者都可能从硝苯地平治疗中获益，但患有雷诺现象的患者可能反应特别好，这可能是由于血管扩张剂可逆性肺血管收缩。另一种假设是，在我们大多数患有雷诺现象的患者中，先前的慢性血管扩张剂治疗保留了肺血管反应性。
