Influence of ACE‐inhibition on salt‐mediated worsening of pulmonary gas exchange in heart failure

Aims  In congestive heart failure (CHF), pulmonary gas exchange, as evaluated by carbon monoxide diffusion (DL_CO), is impaired. ACE‐inhibition improves DL_CO. Infusion of saline worsens DL_CO, because of upregulated sodium and water transport to the alveolar interstitium, which thickens the alveolar–capillary interface and lengthens the diffusion path for gas exchange. We investigated whether enalapril can readjust the capillary permeability to sodium.

Methods  In 10 NYHA class II‐III CHF patients, we measured DL_CO, its two subcomponents (V_C, capillary blood volume available for gas exchange, and D_M, alveolar‐capillary membrane diffusion), left and right ventricular filling pressures, plasma noradrenaline, aldosterone and renin activity, at baseline and following saline infusion in the main pulmonary artery stem, before and after 1 week enalapril treatment (20 mg daily).

Results  Saline (150 ml) significantly reduced DL_CO (−9.1%) and D_M (−9.8%) and augmented V_C (+ 10.7%). Responses to 750 ml saline were somewhat greater and qualitatively similar. Enalapril produced a significant improvement of DL_CO and D_M at rest as well as after saline, that was not associated with variations in ventricular filling pressures, cardiac output and left ventricular ejection fraction, and was not accounted for by humoral changes.

Conclusions  In CHF, ACE‐inhibition attenuates the deterioration of pulmonary gas transfer produced by saline infusion, suggesting an ability to readjust the upregulated sodium transport across the pulmonary microvascular endothelium.

DOI: 10.1046/j.1365-2125.2001.01363.x

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