PMID- 9498945
OWN - NLM
STAT- MEDLINE
DCOM- 19980310
LR  - 20190514
IS  - 0012-3692 (Print)
IS  - 0012-3692 (Linking)
VI  - 113
IP  - 2
DP  - 1998 Feb
TI  - Decreased basal production of nitric oxide in patients with heart disease.
PG  - 317-22
AB  - STUDY OBJECTIVES: 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.
FAU - Sumino, H
AU  - Sumino H
AD  - Second Department of Internal Medicine, Gunma University School of Medicine, 
      Maebashi, Japan. suminoh@news.sb.gunma-u.ac.jp
FAU - Sato, K
AU  - Sato K
FAU - Sakamaki, T
AU  - Sakamaki T
FAU - Masuda, H
AU  - Masuda H
FAU - Nakamura, T
AU  - Nakamura T
FAU - Kanda, T
AU  - Kanda T
FAU - Nagai, R
AU  - Nagai R
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Chest
JT  - Chest
JID - 0231335
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - S88TT14065 (Oxygen)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Blood Pressure/physiology
MH  - Cardiac Output/physiology
MH  - Cardiac Output, Low/metabolism
MH  - Cardiomyopathy, Dilated/metabolism
MH  - Female
MH  - Forced Expiratory Volume
MH  - Heart Diseases/*metabolism
MH  - Hemodynamics/physiology
MH  - Humans
MH  - Lung/blood supply/*metabolism
MH  - Male
MH  - Middle Aged
MH  - Mitral Valve Stenosis/metabolism
MH  - Myocardial Ischemia/metabolism
MH  - Nitric Oxide/*metabolism/physiology
MH  - Oxygen/blood
MH  - Partial Pressure
MH  - Pulmonary Artery/physiopathology
MH  - Pulmonary Circulation/physiology
MH  - Pulmonary Wedge Pressure/physiology
MH  - Spirometry
MH  - Time Factors
MH  - Vascular Resistance/physiology
MH  - Vital Capacity
EDAT- 1998/03/14 00:00
MHDA- 1998/03/14 00:01
CRDT- 1998/03/14 00:00
PHST- 1998/03/14 00:00 [pubmed]
PHST- 1998/03/14 00:01 [medline]
PHST- 1998/03/14 00:00 [entrez]
AID - S0012-3692(16)32408-4 [pii]
AID - 10.1378/chest.113.2.317 [doi]
PST - ppublish
SO  - Chest. 1998 Feb;113(2):317-22. doi: 10.1378/chest.113.2.317.