Boschetti E, Tantucci C, Cocchieri M, Fornari G, Grassi V, Sorbini C A
Respiration. 1985;48(4):296-302. doi: 10.1159/000194843.
The present study was carried out to test the hypothesis of a possible effectiveness of captopril--an enzymatic inhibitor of both angiotensin II formation and bradykinin degradation--on hypoxic pulmonary hypertension. In 6 patients with this clinical condition, captopril-induced changes in pulmonary hemodynamics were observed after the acute administration of the drug with and without a short period of oxygen therapy at a flow rate sufficient to keep the PaO2 over 60 mm Hg. In our patients, captopril significantly lowered pulmonary arterial pressure and vascular resistance only when combined with oxygen, suggesting that an increase in bradykinin availability and/or a decrease in angiotensin II synthesis might be important factors in reversing pulmonary arterial hypertension only after blunting of the hypoxic stimulus on pulmonary circulation. Moreover, the authors suggest that the employment of vasodilators in the setting of hypoxic pulmonary hypertension should be considered not only as a means of relieving vasoconstriction but also as a possible tool for maintaining cardiac output and, in turn, peripheral oxygen delivery.
本研究旨在验证卡托普利（一种同时抑制血管紧张素II生成和缓激肽降解的酶抑制剂）对缺氧性肺动脉高压可能有效的假设。在6例患有这种临床病症的患者中，在急性给予该药物时，观察了有无短时间以足以使动脉血氧分压（PaO2）维持在60 mmHg以上的流速进行氧疗情况下卡托普利引起的肺血流动力学变化。在我们的患者中，卡托普利仅在与氧气联合使用时才显著降低肺动脉压和血管阻力，这表明缓激肽可用性增加和/或血管紧张素II合成减少可能仅是在减弱对肺循环的缺氧刺激后才是逆转肺动脉高压的重要因素。此外，作者认为在缺氧性肺动脉高压情况下使用血管扩张剂不仅应被视为缓解血管收缩的一种手段，而且还应被视为维持心输出量进而维持外周氧输送的一种可能工具。
