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Influence of ACE‐inhibition on salt‐mediated worsening of pulmonary gas exchange in heart failure
Author(s) -
Guazzi Marco,
Brambilla Roberto,
Agostoni Piergiuseppe,
Guazzi Maurizio D.
Publication year - 2001
Publication title -
british journal of clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.216
H-Index - 146
eISSN - 1365-2125
pISSN - 0306-5251
DOI - 10.1046/j.1365-2125.2001.01363.x
Subject(s) - enalapril , saline , heart failure , medicine , aldosterone , cardiology , pulmonary artery , chemistry , cardiac output , hemodynamics , blood pressure , angiotensin converting enzyme
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.