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Transhepatic lactate gradient in relation to liver ischemia/reperfusion injury during major hepatectomies
Author(s) -
Theodoraki Kassiani,
Arkadopoulos Nikolaos,
Fragulidis George,
Voros Dionysios,
Karapanos Konstantinos,
Markatou Maria,
Kostopanagiotou Georgia,
Smyrniotis Vassilios
Publication year - 2006
Publication title -
liver transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.814
H-Index - 150
eISSN - 1527-6473
pISSN - 1527-6465
DOI - 10.1002/lt.20911
Subject(s) - hyperlactatemia , medicine , lactate dehydrogenase , hepatectomy , ischemia , liver transplantation , vein , artery , dissection (medical) , portal vein , venous blood , cardiology , anesthesia , surgery , transplantation , resection , chemistry , biochemistry , enzyme
Hepatectomies performed under selective hepatic vascular exclusion are associated with a series of events culminating in ischemia/reperfusion injury, a state that shares common characteristics with situations known to result in global or regional hyperlactatemia. Accordingly, we sought to determine whether lactate is released by the liver during hepatic resections performed under blood flow deprivation and what relation this has to a possible systemic hyperlactatemic state. After ethical approval, 14 consecutive patients with resectable liver tumors subjected to hepatectomy under inflow and outflow occlusion of the liver were studied. Lactate concentrations were assessed in simultaneously drawn arterial, portal venous, and hepatic venous blood before liver dissection and 50 minutes postreperfusion. Moreover, the transhepatic lactate gradient (hepatic vein − portal vein) was calculated to see if there was net production or consumption of lactate. Before hepatic dissection, the transhepatic lactate gradient was negative, suggesting consumption by the liver. Fifty minutes after reperfusion, this gradient became significantly positive, demonstrating release of lactate by the liver (0.12 ± 0.31 vs. −0.38 ± 0.30 mmol/L, P < 0.05). The magnitude of lactate release correlated with systemic arterial lactate levels at the same time point (r 2 = 0.63, P < 0.001). A weaker but significant correlation was demonstrated between the transhepatic lactate gradient postreperfusion and systemic arterial lactate levels 24 hours postoperatively (r 2 = 0.41, P = 0.013). A strong correlation between the transhepatic lactate gradient postreperfusion and peak postoperative aspartate aminotransferase values was also demonstrated (r 2 = 0.73, P < 0.001). The liver becomes a net producer of lactate in hepatectomies performed under blood flow deprivation. This lactate release can explain some of the systemic hyperlactatemia seen in this context and relates to the extent of ischemia/reperfusion injury. Liver Transpl 12:1825‐1831, 2006. © 2006 AASLD.