title: Pulmonary vasoconstriction due to impaired nitric oxide production after cardiopulmonary bypass.
abstract: BACKGROUND
  Pulmonary hypertension is a serious complication after cardiopulmonary bypass (CPB). This study tests the hypothesis that CPB provokes oxidant-mediated pulmonary endothelial dysfunction, leading to reduced nitric oxide (NO) production and pulmonary vasoconstriction.
  
  
  METHODS
  Twelve piglets underwent 2 hours of CPB. In 6 of them, CPB prime was supplemented with N-mercaptopropionylglycine and catalase, whereas the others were not treated. Left and right ventricular function were evaluated from end-systolic elastance and Starling analysis. Pulmonary vascular resistance and transpulmonary NO production (measuring NO2-, NO3-) were determined to assess pulmonary endothelial function.
  
  
  RESULTS
  Cardiopulmonary bypass caused a significant increase in pulmonary vascular resistance (83 +/- 12 to 212 +/- 30 dynes.cm-5.s kg-1, p < 0.05), associated with a reduction of NO production (8.8 +/- 1.4 to 2.5 +/- 0.5 mumol/min, p < 0.05) and depressed right ventricular function (56 +/- 12% of control), whereas N-mercaptopropionylglycine and catalase added to the CPB allowed a substantial improvement of these deleterious effects of CPB.
  
  
  CONCLUSIONS
  Cardiopulmonary bypass impairs pulmonary NO production, resulting in pulmonary vasoconstriction and right ventricular dysfunction, which can be reduced by antioxidants. These findings imply the validity of NO inhalation therapy for postoperative pulmonary hypertension as a supplementation of endogenous endothelium-derived relaxing factor.
authors.affiliation: Division of Cardiothoracic Surgery, UCLA School of Medicine, USA.
authors.forename: K
authors.initials: K
authors.lastname: Morita
authors.forename: K
authors.initials: K
authors.lastname: Ihnken
authors.forename: G D
authors.initials: GD
authors.lastname: Buckberg
authors.forename: M P
authors.initials: MP
authors.lastname: Sherman
authors.forename: L J
authors.initials: LJ
authors.lastname: Ignarro
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D002315:Cardiopulmonary Bypass / Q000009:adverse effects; D002374:Catalase / Q000494:pharmacology; D004730:Endothelium, Vascular / Q000378:metabolism / Q000503:physiopathology; D006976:Hypertension, Pulmonary / Q000209:etiology; D009566:Nitrates / Q000097:blood; D009569:Nitric Oxide / Q000096:biosynthesis* / Q000097:blood; D009573:Nitrites / Q000097:blood; D016877:Oxidants / Q000378:metabolism; D011651:Pulmonary Artery / Q000378:metabolism / Q000503:physiopathology*; D013552:Swine; D008625:Tiopronin / Q000494:pharmacology; D014655:Vascular Resistance / Q000187:drug effects; D014661:Vasoconstriction / Q000187:drug effects; D018497:Ventricular Dysfunction, Right / Q000209:etiology; D016277:Ventricular Function, Left / Q000187:drug effects; D016278:Ventricular Function, Right / Q000187:drug effects
chemical_list: D000975:Antioxidants; D009566:Nitrates; D009573:Nitrites; D016877:Oxidants; D009569:Nitric Oxide; D008625:Tiopronin; D002374:Catalase