title: The effect of cardiopulmonary bypass on intestinal and pulmonary endothelial permeability.
abstract: OBJECTIVE
  To quantify simultaneously the pulmonary and gastrointestinal (GI) damage that occurs during uncomplicated surgery requiring cardiopulmonary bypass (CPB), and to examine the relationships between markers of such damage.
  
  
  METHODS
  Prospective, open.
  
  
  METHODS
  Adult ICU of a national referral hospital.
  
  
  METHODS
  Twenty patients undergoing elective CPB surgery.
  
  
  RESULTS
  Pulmonary vascular injury was assessed using the protein accumulation index (PAI), a double isotope technique specific for high permeability pulmonary edema. The relationships of the PAI with percent neutrophils in bronchoalveolar lavage (BAL), serum, and BAL myeloperoxidase (MPO), and bypass time were examined. Splanchnic vascular injury was assessed using tonometry to measure intramucosal pH (pHi) and the ratio of absorbed lactulose to L-rhamnose (L/R ratio) to determine gut mucosal permeability. Positive correlations were observed between bypass time and PAI (r = 0.64, p < 0.01), percent neutrophils in the postoperative BAL and PAI (r = 0.51, p < 0.05), and postoperative serum MPO and PAI (r = 0.77, p < 0.001). The L/R ratio rose significantly following CPB from 0.04 +/- 0.01 in controls to 0.48 +/- 0.05 (p < 0.0001). The L/R ratio in patients who developed a low pHi was 0.59 +/- 0.06 compared with 0.32 +/- 0.07 in those whose pHi remained normal (p < 0.05). No significant correlation between bypass time and pHi (r = -0.3, p = 0.33), bypass time and L/R ratio (r = 0.27, p = 0.26), PAI and L/R ratio (r = 0.2, p = 0.42), PAI and pHi (r = -0.34, p = 0.16), postoperative serum MPO and L/R ratio (r = 0.03, p = 0.90), or postoperative serum MPO and pHi (r = -0.10, p = 0.67) could be demonstrated.
  
  
  CONCLUSIONS
  Pulmonary and GI injury are detectable following uncomplicated CPB. The absence of any relationship between the respective markers of dysfunction suggests that differing pathologic processes are responsible.
authors.affiliation: Unit of Critical Care, National Heart and Lung Institute, London, UK.
authors.forename: D G
authors.initials: DG
authors.lastname: Sinclair
authors.forename: P L
authors.initials: PL
authors.lastname: Haslam
authors.forename: G J
authors.initials: GJ
authors.lastname: Quinlan
authors.forename: J R
authors.initials: JR
authors.lastname: Pepper
authors.forename: T W
authors.initials: TW
authors.lastname: Evans
mesh_terms: D001021:Aortic Valve; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry / Q000166:cytology; D002199:Capillary Permeability / Q000502:physiology*; D002315:Cardiopulmonary Bypass / Q000009:adverse effects*; D016022:Case-Control Studies; D001026:Coronary Artery Bypass; D004730:Endothelium, Vascular / Q000503:physiopathology; D005260:Female; D005767:Gastrointestinal Diseases / Q000209:etiology* / Q000503:physiopathology; D006350:Heart Valve Prosthesis; D006801:Humans; D006863:Hydrogen-Ion Concentration; D007362:Intensive Care Units; D007408:Intestinal Absorption / Q000502:physiology; D007422:Intestines / Q000098:blood supply*; D007511:Ischemia / Q000209:etiology*; D008297:Male; D008875:Middle Aged; D018375:Neutrophil Activation; D009195:Peroxidase / Q000378:metabolism; D011446:Prospective Studies; D012128:Respiratory Distress Syndrome / Q000209:etiology* / Q000503:physiopathology
chemical_list: D009195:Peroxidase