Improvement of alveolar-capillary membrane diffusing capacity with enalapril in chronic heart failure and counteracting effect of aspirin

Research output: Contribution to journalArticle

Abstract

Background: KII ACE, the enzyme that converts angiotensin I and inactivates bradykinin, is highly concentrated in the lungs; its blockade reduces exposure to angiotensin II and enhances exposure to prostaglandins generated by local kinin hyperconcentration. Our hypothesis is that ACE inhibitors improve pulmonary function in chronic heart failure (CHF) by readjusting lung vessel tone and permeability or alveolar-capillary membrane diffusion. Methods and Results: In 16 CHF patients and 16 normal volunteers or mild untreated hypertensives, pulmonary function and exercise tests with respiratory gas analysis were assessed on placebo, enalapril (10 mg BID), enalapril plus aspirin (325 mg/d), or aspirin, in random order and double blind, for 15 days each. In CHF, enalapril increased pulmonary carbon monoxide diffusion (DLCO), oxygen consumption (V̇O2), and exercise tolerance and reduced the ratio of dead space to tidal volume (VO/VT) and the ventilatory equivalent for carbon dioxide production (V̇/V̇CO2). On enalapril, V̇O2 (r=80, P2; amelioration in V̇O2 and VD/VT was unrelated to DLCO and was not modified by aspirin. Conclusions: ACE inhibition improved pulmonary diffusion in CHF. Hydralazine-isosorbide dinitrate failed to provide this result. Counteraction by aspirin, a prostaglandin inhibitor, bespeaks prostaglandin participation while on enalapril that might readjust capillary permeability or alveolar-capillary membrane diffusion.

Original languageEnglish
Pages (from-to)1930-1936
Number of pages7
JournalCirculation
Volume95
Issue number7
Publication statusPublished - Apr 1 1997

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Enalapril
Aspirin
Heart Failure
Lung
Membranes
Prostaglandins
Isosorbide Dinitrate
Prostaglandin Antagonists
Hydralazine
Angiotensin I
Kinins
Exercise Tolerance
Respiratory Function Tests
Tidal Volume
Capillary Permeability
Bradykinin
Carbon Monoxide
Exercise Test
Angiotensin-Converting Enzyme Inhibitors
Carbon Dioxide

Keywords

  • angiotensin
  • aspirin
  • prostaglandins
  • respiration
  • vasodilatation

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

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title = "Improvement of alveolar-capillary membrane diffusing capacity with enalapril in chronic heart failure and counteracting effect of aspirin",
abstract = "Background: KII ACE, the enzyme that converts angiotensin I and inactivates bradykinin, is highly concentrated in the lungs; its blockade reduces exposure to angiotensin II and enhances exposure to prostaglandins generated by local kinin hyperconcentration. Our hypothesis is that ACE inhibitors improve pulmonary function in chronic heart failure (CHF) by readjusting lung vessel tone and permeability or alveolar-capillary membrane diffusion. Methods and Results: In 16 CHF patients and 16 normal volunteers or mild untreated hypertensives, pulmonary function and exercise tests with respiratory gas analysis were assessed on placebo, enalapril (10 mg BID), enalapril plus aspirin (325 mg/d), or aspirin, in random order and double blind, for 15 days each. In CHF, enalapril increased pulmonary carbon monoxide diffusion (DLCO), oxygen consumption (V̇O2), and exercise tolerance and reduced the ratio of dead space to tidal volume (VO/VT) and the ventilatory equivalent for carbon dioxide production (V̇/V̇CO2). On enalapril, V̇O2 (r=80, P2; amelioration in V̇O2 and VD/VT was unrelated to DLCO and was not modified by aspirin. Conclusions: ACE inhibition improved pulmonary diffusion in CHF. Hydralazine-isosorbide dinitrate failed to provide this result. Counteraction by aspirin, a prostaglandin inhibitor, bespeaks prostaglandin participation while on enalapril that might readjust capillary permeability or alveolar-capillary membrane diffusion.",
keywords = "angiotensin, aspirin, prostaglandins, respiration, vasodilatation",
author = "Marco Guazzi and Giancarlo Marenzi and Marina Alimento and Mauro Contini and Piergiuseppe Agostoni",
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journal = "Circulation",
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TY - JOUR

T1 - Improvement of alveolar-capillary membrane diffusing capacity with enalapril in chronic heart failure and counteracting effect of aspirin

AU - Guazzi, Marco

AU - Marenzi, Giancarlo

AU - Alimento, Marina

AU - Contini, Mauro

AU - Agostoni, Piergiuseppe

PY - 1997/4/1

Y1 - 1997/4/1

N2 - Background: KII ACE, the enzyme that converts angiotensin I and inactivates bradykinin, is highly concentrated in the lungs; its blockade reduces exposure to angiotensin II and enhances exposure to prostaglandins generated by local kinin hyperconcentration. Our hypothesis is that ACE inhibitors improve pulmonary function in chronic heart failure (CHF) by readjusting lung vessel tone and permeability or alveolar-capillary membrane diffusion. Methods and Results: In 16 CHF patients and 16 normal volunteers or mild untreated hypertensives, pulmonary function and exercise tests with respiratory gas analysis were assessed on placebo, enalapril (10 mg BID), enalapril plus aspirin (325 mg/d), or aspirin, in random order and double blind, for 15 days each. In CHF, enalapril increased pulmonary carbon monoxide diffusion (DLCO), oxygen consumption (V̇O2), and exercise tolerance and reduced the ratio of dead space to tidal volume (VO/VT) and the ventilatory equivalent for carbon dioxide production (V̇/V̇CO2). On enalapril, V̇O2 (r=80, P2; amelioration in V̇O2 and VD/VT was unrelated to DLCO and was not modified by aspirin. Conclusions: ACE inhibition improved pulmonary diffusion in CHF. Hydralazine-isosorbide dinitrate failed to provide this result. Counteraction by aspirin, a prostaglandin inhibitor, bespeaks prostaglandin participation while on enalapril that might readjust capillary permeability or alveolar-capillary membrane diffusion.

AB - Background: KII ACE, the enzyme that converts angiotensin I and inactivates bradykinin, is highly concentrated in the lungs; its blockade reduces exposure to angiotensin II and enhances exposure to prostaglandins generated by local kinin hyperconcentration. Our hypothesis is that ACE inhibitors improve pulmonary function in chronic heart failure (CHF) by readjusting lung vessel tone and permeability or alveolar-capillary membrane diffusion. Methods and Results: In 16 CHF patients and 16 normal volunteers or mild untreated hypertensives, pulmonary function and exercise tests with respiratory gas analysis were assessed on placebo, enalapril (10 mg BID), enalapril plus aspirin (325 mg/d), or aspirin, in random order and double blind, for 15 days each. In CHF, enalapril increased pulmonary carbon monoxide diffusion (DLCO), oxygen consumption (V̇O2), and exercise tolerance and reduced the ratio of dead space to tidal volume (VO/VT) and the ventilatory equivalent for carbon dioxide production (V̇/V̇CO2). On enalapril, V̇O2 (r=80, P2; amelioration in V̇O2 and VD/VT was unrelated to DLCO and was not modified by aspirin. Conclusions: ACE inhibition improved pulmonary diffusion in CHF. Hydralazine-isosorbide dinitrate failed to provide this result. Counteraction by aspirin, a prostaglandin inhibitor, bespeaks prostaglandin participation while on enalapril that might readjust capillary permeability or alveolar-capillary membrane diffusion.

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