title: Effects of ischemia on pulmonary dysfunction after cardiopulmonary bypass.
abstract: BACKGROUND
  Pulmonary hypertension and lung injury secondary to cardiopulmonary bypass (CPB) are probably caused by a combination of ischemia and inflammation. This study was undertaken to investigate the potential ischemic effects of cessation of pulmonary arterial flow during CPB on pulmonary injury.
  
  
  METHODS
  Twenty neonatal piglets (2.5 to 3.1 kg) were randomly assigned to two groups. Group A (n = 10) underwent 90 minutes of CPB at full flow (100 mL x kg(-1) x min(-1)) and clamping of the main pulmonary artery (PA). Group B (n = 10) underwent 90 minutes of partial CPB (66 mL x kg(-1) x min(-1)) with continued mechanical ventilation and without clamping of the PA. All hearts were instrumented with micromanometers and a PA ultrasonic flow probe. Endothelial function was assessed by measuring endothelial-dependent relaxation (measured by change in pulmonary vascular resistance after PA infusion of acetylcholine) and endothelial-independent relaxation (measured by change in pulmonary vascular resistance after ventilator infusion of nitric oxide and PA infusion of sodium nitroprusside).
  
  
  RESULTS
  All groups exhibited signs of pulmonary injury after CPB as evidenced by significantly increased pulmonary vascular resistance, increased alveolar-arterial O2 gradients, and decreased pulmonary compliance (p<0.05); however, pulmonary injury was significantly worse in group A (p<0.05).
  
  
  CONCLUSIONS
  This study suggests that although exposure to CPB alone is enough to cause pulmonary injury, cessation of PA flow during CPB contributes significantly to this pulmonary dysfunction.
authors.affiliation: Department of Surgery, Duke University Medical Center, Durham, North Carolina 27710, USA.
authors.forename: P J
authors.initials: PJ
authors.lastname: Chai
authors.forename: J A
authors.initials: JA
authors.lastname: Williamson
authors.forename: A J
authors.initials: AJ
authors.lastname: Lodge
authors.forename: C W
authors.initials: CW
authors.lastname: Daggett
authors.forename: J E
authors.initials: JE
authors.lastname: Scarborough
authors.forename: J N
authors.initials: JN
authors.lastname: Meliones
authors.forename: I M
authors.initials: IM
authors.lastname: Cheifetz
authors.forename: J J
authors.initials: JJ
authors.lastname: Jaggers
authors.forename: R M
authors.initials: RM
authors.lastname: Ungerleider
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D000831:Animals, Newborn; D002315:Cardiopulmonary Bypass / Q000009:adverse effects*; D004730:Endothelium, Vascular / Q000187:drug effects / Q000503:physiopathology; D006976:Hypertension, Pulmonary / Q000209:etiology / Q000503:physiopathology; D007511:Ischemia / Q000209:etiology* / Q000503:physiopathology; D008168:Lung / Q000098:blood supply* / Q000503:physiopathology*; D008170:Lung Compliance; D009569:Nitric Oxide / Q000494:pharmacology; D011651:Pulmonary Artery / Q000502:physiology; D011652:Pulmonary Circulation; D011659:Pulmonary Gas Exchange; D013552:Swine; D014655:Vascular Resistance / Q000187:drug effects
chemical_list: D009569:Nitric Oxide; D000109:Acetylcholine