结缔组织病合并肺动脉高压患者急性血管扩张试验应用腺苷与伊洛前列素的比较

Comparison of adenosine versus iloprost by acute vasodilator test in patients of pulmonary arterial hypertension complicated with connective tissue diseases

目的比较腺苷和伊洛前列素对结缔组织病合并肺动脉高压（PAH）患者血液动力学的影响和急性血管扩张效应。方法对18例结缔组织病合并PAH患者进行右心导管检查，分别以静脉泵入腺苷和和雾化吸入伊洛前列素的方式进行急性血管扩张试验。用药前后分别测定血液动力学参数。结果与基线值相比，18例患者静脉泵入腺苷后肺动脉收缩压和肺小动脉阻力均明显下降[（71±30）比（80±29）mmHg（1mmHg=0．133kPa），（712±440）比（824±464）dyn·s·cm^-5，均P〈0．05]，心率明显增快[（93±17）比（83±16）次．／min，P〈0．05]；吸入伊洛前列素后肺动脉收缩压、平均压和肺小动脉阻力均明显下降[（66±29）比（79±28）mmHg，（43±19）比（52±19）mmHg，（632±440）比（816±448）dyn·s·cm^-5，均P〈0．05），而且肺动脉平均压和肺小血管阻力明显低于泵人腺苷后（均P〈0．05），心率无明显变化[（82±16）比（82±16）次／min，P〉0．05]。2种药物对心排血量、经皮血氧饱和度和体循环血压均无明显影响。使用腺苷时因副作用导致终止用药者5例（28％），而使用伊洛前列素无一例终止用药。结论在结缔组织病合并PAH患者中，静脉泵入腺苷和吸人伊洛前列素具有相似的血液动力学效应。吸入伊洛前列素能够更明显地减低肺动脉收缩压和肺小动脉阻力，而且副作用更少。

Objective To compare the acute hemodynamic effects of adenosine versus iloprost in patients of pulmonary arterial hypertension （PAH） complicated with connective tissue diseases. Methods During right heart catheterization, 18 patients of PAH complicated with connective tissue diseases sequentially received intravenous infusion of adenosine and inhaled iloprost. After the baseline hemodynamic data were obtained, an adenosine infusion was started and titrated to the maximal tolerated dose. The hemodynamic parameters were allowed to return to baseline. Then inhalation of iloprost was administered. The effects of both medicines on the patient＇s hemodynamics were monitored. Results As compared with the baseline values, the systolic pulmonary artery pressure and pulmonary vascular resistance significantly decreased [ （71 ±30） vs （80 ±29） mm Hg and （712 ±440） vs （824 ±464） dyn . s . cm^-5 respectively, both P 〈 0.05 ） while the heart rate increased significantly [ （93 ± 17 ） vs （ 83 ± 16 ） beat/min, P 〈 0.05 ] in the adenosine group. Inhaled iloprost could also lower the systolic pulmonary artery pressure [ （66 ± 29 ） vs （79 ± 28） mm Hg, P 〈 0.05 ] , mean pulmonary artery pressure [ （43 ± 19） vs （52 ± 19） mm Hg, P 〈 0. 05 ] and pulmonary vascular resistance [ （ 632 ± 440） v s （ 816 ± 448 ） dyn . s . cm^-5, p 〈 0.05 ] without any effect upon heart rate. Inhaled iloprost exerted more potent effect on lowering mean pulmonary artery pressure and pulmonary vascular resistance than adenosine （ P 〈 0.05 ）. The two medicines did not affect cardiac output, pulse oxygen saturation or systemic blood pressure. The side effects were fewer in the iloprost inhalation group than the adenosine group. Conclusion During acute vasodilator testing, inhaled iloprost was more potent than infused adenosine as a pulmonary vasodilator in PAH complicated with connective tissue diseases.