title: Serum acidosis prior to reperfusion facilitates hemodynamic recovery following liver transplantation.
abstract: BACKGROUND
  Reperfusion is the most critical event during liver transplantation, and sustained leakage of acidic preservation solution from the liver graft contributes to marked hemodynamic instability. Recent laboratory studies with hepatocyte cultures have revealed that low pH may protect hepatocyte mitochondria against ischemia-reperfusion injury by inhibiting the mitochondrial permeability transition (MPT), the so-called "pH paradox." However, the clinical significance of this pH paradox theory remains largely unknown. In this study, we sought to determine whether there is an association between serum pH immediately prior to reperfusion and hemodynamic recovery after reperfusion and graft survival.
  
  
  METHODS
  We analyzed retrospective data from 527 patients who underwent Orthotopic liver transplantation between 2003 and 2008. All patients were allocated to one of two groups: pH ≤ 7.32 or pH > 7.32, as measured 5 min before reperfusion. Case-control matching was performed using the propensity score to adjust for background differences between the two groups. Data were analyzed using Student's t-test and the χ (2) test.
  
  
  RESULTS
  There were 85 patients in the pH ≤ 7.32 group and 385 patients in the pH > 7.32 group. The recovery of mean arterial pressure after hepatic artery reperfusion was significantly faster in the pH ≤ 7.32 group (slope of recovery: 0.0004 % vs. 0.0002 %/min, p = 0.041). Other parameters studied, including vasopressor dosage after reperfusion, did not show any statistically significant difference between groups.
  
  
  CONCLUSIONS
  Our findings suggest that less aggressive treatment of acidosis with a slower rate of normalization of serum pH (from low to normal) after reperfusion promotes faster hemodynamic stabilization. These findings provide evidence to support the concept of the pH paradox, and may also substantiate the argument against the usage of alkalizing agents before reperfusion unless acidosis becomes clinically significant.
authors.affiliation: Division of Transplant Anesthesia, Department of Anesthesiology and Pain Medicine, University of Washington, School of Medicine, 1959 NE Pacific Street, Seattle, WA, 98195, USA. fukazawa@uw.edu.
authors.forename: Kyota
authors.initials: K
authors.lastname: Fukazawa
authors.affiliation: Division of Transplant Anesthesia, Department of Anesthesiology and Pain Medicine, University of Washington, School of Medicine, 1959 NE Pacific Street, Seattle, WA, 98195, USA.
authors.forename: Alexander A
authors.initials: AA
authors.lastname: Vitin
authors.affiliation: Division of Solid Organ Transplantation, Department of Anesthesiology, University of Miami, Leonard Miller School of Medicine, Miami, FL, USA.
authors.forename: Ernesto A
authors.initials: EA
authors.lastname: Pretto
mesh_terms: D000138:Acidosis / Q000097:blood*; D000328:Adult; D000368:Aged; D005260:Female; D006439:Hemodynamics; D022781:Hepatocytes / Q000378:metabolism; D006801:Humans; D016031:Liver Transplantation / Q000379:methods*; D008297:Male; D008875:Middle Aged; D015424:Reperfusion; D015427:Reperfusion Injury / Q000503:physiopathology*; D012189:Retrospective Studies; D014662:Vasoconstrictor Agents / Q000008:administration & dosage*
chemical_list: D014662:Vasoconstrictor Agents
keywords: Acidosis; Liver transplantation; Organ transplant; Reperfusion