title: Hemodynamic effects of inhaled nitric oxide in heart failure.
abstract: OBJECTIVE
  This study was performed to assess the utility of inhaled nitric oxide as a selective pulmonary vasodilator in patients with severe chronic heart failure and to compare its hemodynamic effects with those of nitroprusside, a nonselective vasodilator.
  
  
  BACKGROUND
  Preoperative pulmonary vascular resistance is a predictor of right heart failure after heart transplantation. Non-selective vasodilators administered preoperatively to assess the reversibility of pulmonary vasoconstriction cause systemic hypotension, limiting their utility.
  
  
  METHODS
  Systemic and pulmonary hemodynamic measurement were made at baseline, during oxygen inhalation and with the addition of graded doses of inhaled nitric oxide or intravenous nitroprusside in 16 patients with New York Heart Association class III or IV heart failure referred for heart transplantation.
  
  
  RESULTS
  Pulmonary vascular resistance decreased to a greater extent with 80 ppm nitric oxide (mean +/- SEM 256 +/- 41 to 139 +/- 14 dynes.s.cm-5) than with the maximally tolerated dose of nitroprusside (264 +/- 49 to 169 +/- 30 dynes.s.cm-5, p < 0.05, nitric oxide vs. nitroprusside). Pulmonary capillary wedge pressure increased with 80 ppm nitric oxide (26 +/- 2 to 32 +/- 2 mm Hg, p < 0.05). Mean arterial pressure did not change with nitric oxide but decreased with nitroprusside. Seven of the 16 patients, including 1 patient who did not have an adequate decrease in pulmonary vascular resistance with nitroprusside but did with nitric oxide, have undergone successful heart transplantation.
  
  
  CONCLUSIONS
  Inhaled nitric oxide is a selective pulmonary vasodilator in patients with pulmonary hypertension due to left heart failure and may identify patients with reversible pulmonary vasoconstriction in whom agents such as nitroprusside cause systemic hypotension. Inhaled nitric oxide causes an increase in left ventricular filling pressure by an unknown mechanism.
authors.affiliation: Department of Medicine, Massachusetts General Hospital, Boston 02114.
authors.forename: M J
authors.initials: MJ
authors.lastname: Semigran
authors.forename: B A
authors.initials: BA
authors.lastname: Cockrill
authors.forename: R
authors.initials: R
authors.lastname: Kacmarek
authors.forename: B T
authors.initials: BT
authors.lastname: Thompson
authors.forename: W M
authors.initials: WM
authors.lastname: Zapol
authors.forename: G W
authors.initials: GW
authors.lastname: Dec
authors.forename: M A
authors.initials: MA
authors.lastname: Fifer
mesh_terms: D000280:Administration, Inhalation; D000328:Adult; D001794:Blood Pressure / Q000187:drug effects; D002908:Chronic Disease; D005260:Female; D006333:Heart Failure / Q000188:drug therapy* / Q000503:physiopathology / Q000601:surgery; D016027:Heart Transplantation; D006439:Hemodynamics / Q000187:drug effects*; D006801:Humans; D007262:Infusions, Intravenous; D008297:Male; D008875:Middle Aged; D009569:Nitric Oxide / Q000008:administration & dosage / Q000627:therapeutic use*; D009599:Nitroprusside / Q000008:administration & dosage / Q000494:pharmacology; D011652:Pulmonary Circulation / Q000187:drug effects; D011669:Pulmonary Wedge Pressure / Q000187:drug effects; D012044:Regression Analysis; D014655:Vascular Resistance / Q000187:drug effects; D014661:Vasoconstriction / Q000187:drug effects; D014665:Vasodilator Agents / Q000008:administration & dosage / Q000627:therapeutic use
chemical_list: D014665:Vasodilator Agents; D009599:Nitroprusside; D009569:Nitric Oxide