Guazzi M, Agostoni P
Istituto di Cardiologia dell'Università degli Studi, Centro di Studio per le Ricerche Cardiovascolari del Consiglio Nazionale delle Ricerche, Fondazione 'Monzino', I.R.C.C.S., Via C. Parea 4, 20138 Milan, Italy.
Clin Sci (Lond). 1999 Jan;96(1):17-22.
Conductance of alveolar capillary membrane (DM) and capillary blood volume (VC) are the subcomponents of the pulmonary diffusing capacity for carbon monoxide (DLCO). In chronic heart failure, stress failure of the membrane provides a mechanism for reduced DM and subsequent impairment of DLCO. Angiotensin-converting enzyme inhibition improves DLCO in patients with chronic heart failure. This study was aimed at investigating which of the two subcomponents of DLCO is affected by angiotensin-converting enzyme inhibitors. Twenty-seven patients with NYHA class II to III chronic heart failure (group 1) and 13 age- and sex-matched normal subjects underwent pulmonary function testing with determination of DM and VC, while receiving placebo and 48 h and 1 and 2 months after starting enalapril treatment (10 mg twice daily). Nine similar patients (group 2) received isosorbide dinitrate (40 mg thrice daily) for a month then enalapril for another month, and underwent pulmonary function testing at 48 h and 1 month after starting treatments. Effects of angiotensin-converting enzyme inhibition in normal controls were not significant in the short- or mid-term. In group 1 patients, the only change observed at 48 h was a reduction in VC (probably due to a decrease in capillary pulmonary pressure). There was a marked increase in DM to a similar extent at 1 and 2 months, resulting in a significant improvement in DLCO despite a decrease in VC. In group 2 patients, nitrates failed to improve DLCO and DM, whereas enalapril was as effective as in group 1. These observations suggest a modulatory effect of angiotensin-converting enzyme inhibition on the membrane function which emerges gradually and persists over time and is probably dissociated from changes in pulmonary capillary pressure and VC. Chronic heart failure disturbs the alveolar capillary interface and increases gas diffusion resistance; angiotensin-converting enzyme inhibition restores the diffusive properties of the membrane and gas transfer, and protects the lung when the heart is failing.
肺泡毛细血管膜传导率（DM）和毛细血管血容量（VC）是一氧化碳肺弥散量（DLCO）的子成分。在慢性心力衰竭中，膜的应激性衰竭为DM降低及随后的DLCO受损提供了一种机制。血管紧张素转换酶抑制可改善慢性心力衰竭患者的DLCO。本研究旨在调查DLCO的这两个子成分中哪一个受血管紧张素转换酶抑制剂影响。27例纽约心脏协会（NYHA）心功能II至III级的慢性心力衰竭患者（第1组）和13例年龄及性别匹配的正常受试者在接受安慰剂时以及开始依那普利治疗（每日2次，每次10 mg）后48小时、1个月和2个月时进行了肺功能测试，测定DM和VC。9例类似患者（第2组）先接受硝酸异山梨酯（每日3次，每次40 mg）治疗1个月，然后接受依那普利治疗1个月，并在开始治疗后48小时和1个月时进行肺功能测试。血管紧张素转换酶抑制对正常对照者的短期或中期影响不显著。在第1组患者中，48小时时观察到的唯一变化是VC降低（可能是由于肺毛细血管压力降低）。1个月和2个月时DM有显著增加且程度相似，尽管VC降低，但DLCO仍有显著改善。在第2组患者中，硝酸盐未能改善DLCO和DM，而依那普利的效果与第1组相同。这些观察结果表明血管紧张素转换酶抑制对膜功能有调节作用，这种作用逐渐显现并随时间持续存在，可能与肺毛细血管压力和VC的变化无关。慢性心力衰竭会扰乱肺泡毛细血管界面并增加气体扩散阻力；血管紧张素转换酶抑制可恢复膜的扩散特性和气体转运，并在心脏衰竭时保护肺脏。
