Theodoraki Kassiani, Arkadopoulos Nikolaos, Fragulidis George, Voros Dionysios, Karapanos Konstantinos, Markatou Maria, Kostopanagiotou Georgia, Smyrniotis Vassilios
First Department of Anesthesiology, Areteion Hospital, University of Athens School of Medicine, Athens, Greece.
Liver Transpl. 2006 Dec;12(12):1825-31. doi: 10.1002/lt.20911.
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.
在选择性肝血管阻断下进行的肝切除术会引发一系列事件，最终导致缺血/再灌注损伤，这种状态与已知会导致全身性或局部性高乳酸血症的情况具有共同特征。因此，我们试图确定在血流阻断下进行肝切除术期间肝脏是否会释放乳酸，以及这与可能的全身性高乳酸血症状态有何关系。经伦理批准后，对14例连续的可切除肝肿瘤患者进行了研究，这些患者在肝流入和流出道阻断下接受了肝切除术。在肝脏解剖前和再灌注后50分钟，同时采集动脉血、门静脉血和肝静脉血，评估乳酸浓度。此外，计算经肝乳酸梯度（肝静脉 - 门静脉），以观察是否存在乳酸的净生成或消耗。在肝脏解剖前，经肝乳酸梯度为负，表明肝脏在消耗乳酸。再灌注后50分钟，该梯度变为显著正值，表明肝脏释放乳酸（0.12±0.31对-0.38±0.30 mmol/L，P<0.05）。乳酸释放量与同一时间点的全身动脉乳酸水平相关（r² = 0.63，P<0.001）。再灌注后的经肝乳酸梯度与术后24小时的全身动脉乳酸水平之间存在较弱但显著的相关性（r² = 0.41，P = 0.013）。再灌注后的经肝乳酸梯度与术后峰值天冬氨酸转氨酶值之间也存在很强的相关性（r² = 0.73，P<0.001）。在血流阻断下进行的肝切除术中，肝脏成为乳酸的净生成器官。这种乳酸释放可以解释在此情况下出现的部分全身性高乳酸血症，并且与缺血/再灌注损伤的程度有关。
