title: Ischemic preconditioning attenuates lactate release by the liver during hepatectomies under vascular control: a case-control study.
abstract: BACKGROUND
  We have previously demonstrated lactate release by the liver itself in hepatectomies performed under selective hepatic vascular exclusion. We hypothesized that ischemic preconditioning applied in this setting might lead to a reduction of hepatic lactate production.
  
  
  METHODS
  Twenty-one patients underwent hepatectomy under inflow and outflow occlusion combined with ischemic preconditioning (IP group, n = 21). These patients were matched 1:1 with patients subjected to the same technique of hepatectomy under vascular occlusion without ischemic preconditioning (control group, n = 21). The transhepatic lactate gradient (hepatic vein-portal vein) was calculated before liver dissection and 60 min post-reperfusion.
  
  
  RESULTS
  In the control group, the transhepatic lactate gradient before liver resection was negative indicating consumption by the liver. After 60 min post-reperfusion, this gradient became positive, indicating net lactate production by the liver (0.2 ± 0.3 vs. -0.3 ± 0.2 mmol/L, P < 0.001). In the IP group, the liver consumed lactate both before resection and 60 min post-reperfusion (gradients -0.2 ± 1.1 and -0.1 ± 0.6 mmol/L, respectively). The magnitude of lactate release by the liver correlated with systemic hyperlactatemia post-reperfusion and 24 h postoperatively (r(2) = 0.54, P < 0.001 and r(2) = 0.67, P < 0.001, respectively). Significant correlations between the transhepatic lactate gradient post-reperfusion and peak postoperative AST as well as the apoptotic response of the liver remnant were also demonstrated (r(2) = 0.72, P < 0.001 and r(2) = 0.66, P < 0.001, respectively).
  
  
  CONCLUSIONS
  The microcirculatory derangement and cellular aerobic metabolism breakdown elicited by ischemia-reperfusion insults can be prevented with hepatoprotective measures such as ischemic preconditioning. The transhepatic lactate gradient could act as a monitoring and prognostic tool of the efficacy of ischemic preconditioning.
authors.affiliation: First Department of Anesthesiology, Areteion Hospital, University of Athens School of Medicine, Lambaki 61-63, Athens 111 43, Greece. ktheodoraki@hotmail.com
authors.forename: Kassiani
authors.initials: K
authors.lastname: Theodoraki
authors.forename: Nikolaos
authors.initials: N
authors.lastname: Arkadopoulos
authors.forename: George
authors.initials: G
authors.lastname: Fragulidis
authors.forename: Ioannis
authors.initials: I
authors.lastname: Vassiliou
authors.forename: Maria
authors.initials: M
authors.lastname: Markatou
authors.forename: Agatha
authors.initials: A
authors.lastname: Pafiti
authors.forename: Georgia
authors.initials: G
authors.lastname: Kostopanagiotou
authors.forename: Vassilios
authors.initials: V
authors.lastname: Smyrniotis
mesh_terms: D000328:Adult; D000368:Aged; D001219:Aspartate Aminotransferases / Q000097:blood; D016022:Case-Control Studies; D005260:Female; D006498:Hepatectomy; D006801:Humans; D019194:Ischemic Preconditioning; D019344:Lactic Acid / Q000097:blood*; D008099:Liver / Q000098:blood supply* / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D010100:Oxygen / Q000097:blood
chemical_list: D019344:Lactic Acid; D001219:Aspartate Aminotransferases; D010100:Oxygen