| Nitric oxide production during exercise in chronic heart failure. | |
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MedLine Citation:
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PMID: 9313597 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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In chronic heart failure (CHF), the ventilatory response is increased compared with normal. This response is, in part, caused by reduced perfusion to ventilated lung. Nitric oxide (NO) is a potent vasodilator and may have an important role in pulmonary vasodilatation during exercise. NO is present in exhaled air. The amount of NO in exhaled air, when breathing NO-free compressed air, is known to increase in normal subjects during exercise. In this study, we quantified NO output in exhaled air in patients with CHF during exercise. Six patients with CHF (New York Heart Association Class II and III; two with dilated cardiomyopathy, three with ischemic heart disease, and one with hypertensive heart disease) and six normal subjects were studied with a symptom-limited incremental exercise test on a cycle ergometer. Oxygen uptake (VO2), carbon dioxide output (VCO2), and minute ventilation (VE) were measured breath by breath with a mass spectrometer, flow meter, and computer. The NO concentration was continuously measured in mixed expired air by chemiluminescence. Peak exercise work rate was lower in patients with CHF than in normal subjects (71.3 +/- 41.6 W vs 257.0 +/- 49.7 W; p < 0.01). Patients with CHF showed a higher VE/VCO2 level at peak exercise than normal subjects (CHF, 47.0 +/- 10.7; normal subjects, 35.6 +/- 5.2; p < 0.01). NO concentration of exhaled air at rest was lower in CHF patients than in normal subjects (4.0 +/- 2.2 ppb vs 10.5 +/- 6.2 ppb, respectively; p < 0.05). NO output from the respiratory tract (VNO) was significantly lower in patients with CHF compared with normal subjects at rest (45.3 +/- 24.3 nl/min, 117.5 +/- 60.1 nl/min, respectively, p < 0.05), and although it increased during exercise, it did not increase in patients with CHF as much as in normal subjects (75.3 +/- 43.4 nl/min vs 512.9 +/- 253.6 nl/min, respectively; p < 0.01). The increase above rest (exercise/rest) was smaller in patients with CHF than in normal subjects (2.10 +/- 1.92 vs 4.81 +/- 2.67, p < 0.05). These data support the concept that the smaller increase in NO production (VNO) during exercise may be responsible for a blunted vasodilation in patients with CHF, resulting in a smaller reduction in dead space/tidal volume and VE/VCO2 at the lactic acidosis threshold than normal. This finding may play a role in the abnormally high ventilatory response to exercise in patients with CHF. |
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Authors:
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H Adachi; P H Nguyen; R Belardinelli; D Hunter; T Jung; K Wasserman |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: American heart journal Volume: 134 ISSN: 0002-8703 ISO Abbreviation: Am. Heart J. Publication Date: 1997 Aug |
Date Detail:
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Created Date: 1997-10-16 Completed Date: 1997-10-16 Revised Date: 2006-02-27 |
Medline Journal Info:
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Nlm Unique ID: 0370465 Medline TA: Am Heart J Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 196-202 Citation Subset: AIM; IM |
Affiliation:
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Division of Respiratory and Critical Care Physiology and Medicine, Harbor-UCLA Medical Center, Torrance, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adult Breath Tests Cardiac Output, Low / etiology, metabolism*, physiopathology Cardiomyopathy, Dilated / metabolism, physiopathology Chronic Disease Exercise / physiology* Exercise Test Humans Hypertension / complications, metabolism, physiopathology Middle Aged Myocardial Ischemia / complications, metabolism, physiopathology Nitric Oxide / analysis, biosynthesis* Pulmonary Gas Exchange Reference Values |
| Chemical | |
Reg. No./Substance:
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10102-43-9/Nitric Oxide |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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