title: Decreased basal production of nitric oxide in patients with heart disease.
abstract: OBJECTIVE
  The pathophysiologic role of nitric oxide (NO) released in the lung is not well understood. To determine whether the production of endogenous NO is correlated with any hemodynamic parameters, we measured the amount of NO released from the lung tissue of patients with heart disease.
  
  
  METHODS
  Twenty patients (14 with ischemic heart disease, 4 with dilated cardiomyopathy, and 2 with mitral stenosis) and 16 normal control subjects were enrolled in the study. We measured exhaled air samples by using a method developed in our laboratory. The NO release rate from the lungs was calculated from the amount of exhaled NO and the duration of the exhalation.
  
  
  RESULTS
  The rate of NO release was significantly lower in the patients with moderate-to-severe heart failure (New York Heart Association [NYHA] II or III) than in those with mild heart failure (NYHA I) or in normal control subjects. The rate of NO release was positively correlated with the cardiac index (r=0.50, p<0.05), and was negatively correlated with either the systemic (r= -0.58, p<0.01) or pulmonary vascular resistance (r=-0.45, p<0.05). In the patients with moderate-to-severe heart failure, the amount of NO released and the oxygen tension in the pulmonary artery were significantly lower compared with those parameters in patients with mild heart failure.
  
  
  CONCLUSIONS
  Results suggest that the basal production of endogenous NO in the lung tissue of patients with heart failure is impaired, perhaps leading to the elevated pulmonary vascular tone seen in patients with moderate-to-severe heart failure.
authors.affiliation: Second Department of Internal Medicine, Gunma University School of Medicine, Maebashi, Japan. suminoh@news.sb.gunma-u.ac.jp
authors.forename: H
authors.initials: H
authors.lastname: Sumino
authors.forename: K
authors.initials: K
authors.lastname: Sato
authors.forename: T
authors.initials: T
authors.lastname: Sakamaki
authors.forename: H
authors.initials: H
authors.lastname: Masuda
authors.forename: T
authors.initials: T
authors.lastname: Nakamura
authors.forename: T
authors.initials: T
authors.lastname: Kanda
authors.forename: R
authors.initials: R
authors.lastname: Nagai
mesh_terms: D000328:Adult; D000368:Aged; D001794:Blood Pressure / Q000502:physiology; D002302:Cardiac Output / Q000502:physiology; D002303:Cardiac Output, Low / Q000378:metabolism; D002311:Cardiomyopathy, Dilated / Q000378:metabolism; D005260:Female; D005541:Forced Expiratory Volume; D006331:Heart Diseases / Q000378:metabolism*; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D008168:Lung / Q000098:blood supply / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D008946:Mitral Valve Stenosis / Q000378:metabolism; D017202:Myocardial Ischemia / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism* / Q000502:physiology; D010100:Oxygen / Q000097:blood; D010313:Partial Pressure; D011651:Pulmonary Artery / Q000503:physiopathology; D011652:Pulmonary Circulation / Q000502:physiology; D011669:Pulmonary Wedge Pressure / Q000502:physiology; D013147:Spirometry; D013997:Time Factors; D014655:Vascular Resistance / Q000502:physiology; D014797:Vital Capacity
chemical_list: D009569:Nitric Oxide; D010100:Oxygen