title: Nitric oxide synthase expression in lungs of pulmonary hypertensive patients with heart disease.
abstract: Since little is known about the contribution of endothelial nitric oxide synthase (e-NOS) to the mechanism of pulmonary vasospasm and the development of pulmonary vascular occlusive disease, we elucidate how e-NOS is expressed in lung biopsy specimens obtained from operative patients with pulmonary hypertension. Lung biopsy specimens were obtained from 17 patients who underwent open-heart operations for various heart diseases. A piece of normal lung specimen was also obtained from the resected lungs of three lung cancer patients as a control. e-NOS expression was visualized with a monoclonal antibody against e-NOS, and the level of expression was partially quantified. Significantly high levels of e-NOS expression were seen in adult patients, whose preoperative mean pulmonary arterial pressures were greater than 20 mm Hg. In contrast, e-NOS expression in pediatric patients with the same levels of mean pulmonary arterial pressure was the same as that in the controls and in low pulmonary arterial pressure. There was a statistically significant positive correlation between the level of e-NOS expression and Heath--Edwards grading. These data suggest that the e-NOS expression in lung tissue is induced when pulmonary vascular obstructive diseases progress.
authors.affiliation: Department of Thoracic and Cardiovascular Surgery, Wakayama Medical University, 811-1, Kimiidera, Wakayama 641-0012, Japan. komaih@mail.wakayama-med.ac.jp
authors.forename: H
authors.initials: H
authors.lastname: Komai
authors.forename: Y
authors.initials: Y
authors.lastname: Naito
authors.forename: Y
authors.initials: Y
authors.lastname: Aimi
authors.forename: H
authors.initials: H
authors.lastname: Kimura
mesh_terms: D000368:Aged; D001794:Blood Pressure / Q000502:physiology; D006348:Cardiac Surgical Procedures; D002648:Child; D004374:Ductus Arteriosus, Patent / Q000150:complications / Q000201:enzymology / Q000473:pathology / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000201:enzymology / Q000473:pathology; D005260:Female; D006331:Heart Diseases / Q000150:complications / Q000201:enzymology* / Q000473:pathology / Q000503:physiopathology; D006344:Heart Septal Defects, Atrial / Q000150:complications / Q000201:enzymology / Q000473:pathology / Q000503:physiopathology; D006345:Heart Septal Defects, Ventricular / Q000150:complications / Q000201:enzymology / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D006976:Hypertension, Pulmonary / Q000201:enzymology* / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D007124:Immunoenzyme Techniques; D007223:Infant; D008168:Lung / Q000098:blood supply / Q000201:enzymology* / Q000473:pathology; D008297:Male; D008875:Middle Aged; D008944:Mitral Valve Insufficiency / Q000150:complications / Q000201:enzymology / Q000473:pathology / Q000503:physiopathology; D008946:Mitral Valve Stenosis / Q000150:complications / Q000201:enzymology / Q000473:pathology / Q000503:physiopathology; D019001:Nitric Oxide Synthase / Q000378:metabolism*; D052250:Nitric Oxide Synthase Type III; D011651:Pulmonary Artery / Q000503:physiopathology; D013771:Tetralogy of Fallot / Q000150:complications / Q000201:enzymology / Q000473:pathology / Q000503:physiopathology
chemical_list: C496314:NOS3 protein, human; D019001:Nitric Oxide Synthase; D052250:Nitric Oxide Synthase Type III