Document Detail


Nitric oxide inhalation reduces pulmonary tidal volume during exercise in severe chronic heart failure.
MedLine Citation:
PMID:  9351742     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Multiple mechanisms have been proposed to explain the hyperventilation and the limited exercise capacity in congestive heart failure (CHF) including increased intrapulmonary pressures, total pulmonary resistance, and airway abnormalities. We investigated the hypothesis that inhalation of nitric oxide could influence the maximum exercise capacity and excessive ventilatory response to exercise in CHF. Fifteen patients in CHF (mean age 48 +/- 12 years) underwent a control and a nitric oxide inhalation progressive treadmill exercise test with 30 ppm. We determined the maximum oxygen consumptiom (peak VO2), CO2 production (VCO2), minute pulmonary ventilation (VE), respiratory rate, tidal volume (VT), ventilatory equivalent for oxygen (VE/VO2), ventilatory equivalent for carbon dioxide (VE/VCO2), estimated physiologic dead space/tidal volume ratio (VD/VT), VE/VCO2 slope, heart rate, systemic arterial pressure, VE/exercise time slope, and VT/exercise time slope during every incremental exercise. Mean maximum exercise values of heart rate, systolic systemic arterial pressure, diastolic systemic arterial pressure, VD/VT, respiratory rate, peak VO2, VO2/heart rate, VE/CO2, and maximum exercise time were unchanged by inhalation of nitric oxide. There was a strong trend toward reduction of VE/VO2 from 53 +/- 15 to 47 +/- 12 (p = 0.051) and in maximum VE from 58 +/- 21 to 48 +/- 17 L x min(-1) (p = 0.059). Maximum VT decreased from 1639 +/- 556 to 1406 +/- 479 ml (p = 0.04). The VE/VCO2 slope was reduced from 43 +/- 12 to 35 +/- 8 (p = 0.018). Two patients had signs of pulmonary congestion during peak exercise or the recovery period with inhalation of nitric oxide. The VE/exercise time slope and VT/exercise time slope during incremental exercise were reduced by inhalation of nitric oxide, demonstrating a statistically significant minor increase in VE and VT. Inhalation of nitric oxide attenuated the excessive increase in VT response to exercise in CHF. The L-arginine-nitric oxide pathway may be involved in mechanisms contributing to hyperventilation during exercise in CHF.
Authors:
E A Bocchi; J O Auler; G V Guimarães; M J Carmona; M Wajngarten; G Bellotti; F Pileggi
Publication Detail:
Type:  Clinical Trial; Journal Article; Randomized Controlled Trial    
Journal Detail:
Title:  American heart journal     Volume:  134     ISSN:  0002-8703     ISO Abbreviation:  Am. Heart J.     Publication Date:  1997 Oct 
Date Detail:
Created Date:  1997-11-14     Completed Date:  1997-11-14     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0370465     Medline TA:  Am Heart J     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  737-44     Citation Subset:  AIM; IM    
Affiliation:
Heart Institute, Sâo Paulo University Medical School, Brazil. DCL_EDIMAR@PINATUBO.INCOR.USP.BR
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MeSH Terms
Descriptor/Qualifier:
Administration, Inhalation
Adult
Blood Pressure / drug effects
Chronic Disease
Exercise Test*
Female
Heart Failure / physiopathology*
Heart Rate / drug effects
Humans
Lung / drug effects*,  physiopathology*
Male
Middle Aged
Nitric Oxide / administration & dosage*
Respiratory Function Tests
Severity of Illness Index
Tidal Volume / drug effects*
Chemical
Reg. No./Substance:
10102-43-9/Nitric Oxide

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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