@article{3149143,
    title = "Ischemic Preconditioning Attenuates Lactate Release by the Liver During
Hepatectomies Under Vascular Control: A Case-Control Study",
    author = "Theodoraki, Kassiani and Arkadopoulos, Nikolaos and Fragulidis, George and and Vassiliou, Ioannis and Markatou, Maria and Pafiti, Agatha and and Kostopanagiotou, Georgia and Smyrniotis, Vassilios",
    journal = "Journal of Gastrointestinal Surgery: Official Journal of the Society for Surgery of the Alimentary Tract",
    year = "2011",
    volume = "15",
    number = "4",
    pages = "589-597",
    publisher = "Springer-Verlag",
    issn = "1091-255X, 1873-4626",
    doi = "10.1007/s11605-011-1439-4",
    keywords = "Reperfusion injury; Lactate kinetics; Anaerobic metabolism; Apoptosis;
Hepatoprotection",
    abstract = "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.
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.
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).
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."
}