首页> 外文期刊>Journal of gastrointestinal surgery: official journal of the Society for Surgery of the Alimentary Tract >Ischemic preconditioning attenuates lactate release by the liver during hepatectomies under vascular control: a case-control study.
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Ischemic preconditioning attenuates lactate release by the liver during hepatectomies under vascular control: a case-control study.

机译:缺血预处理在血管控制下的肝切除术中减弱了肝脏释放的乳酸:一项病例对照研究。

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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). CONCLUSION: 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.
机译:背景:我们先前已经证明在选择性肝血管排斥下进行的肝切除术中肝脏自身释放乳酸。我们假设在这种情况下进行缺血预处理可能会导致肝乳酸生成的减少。方法:21例患者在流入和流出闭塞下结合缺血预处理进行了肝切除术(IP组,n = 21)。这些患者与接受相同血管切除术且未进行缺血预处理的肝切除术患者按1:1比例配对(对照组,n = 21)。在肝解剖前和再灌注后60分钟计算经肝乳酸梯度(肝静脉-门静脉)。结果:在对照组中,肝切除前的经肝乳酸梯度为负,表明被肝脏消耗。再灌注后60分钟后,该梯度变为正值,表明肝脏产生的乳酸净含量(0.2 +/- 0.3对-0.3 +/- 0.2 mmol / L,P <0.001)。在IP组中,肝脏在切除前和再灌注后60分钟均消耗乳酸(梯度分别为-0.2 +/- 1.1和-0.1 +/- 0.6 mmol / L)。肝脏释放乳酸的量与再灌注后和术后24 h全身性高乳酸血症相关(r(2)= 0.54,P <0.001和r(2)= 0.67,P <0.001)。还证实了经肝乳酸梯度再灌注后与峰值AST以及肝残余细胞的凋亡反应之间的显着相关性(r(2)= 0.72,P <0.001和r(2)= 0.66,P <0.001,分别)。结论:缺血再灌注等肝保护措施可预防缺血再灌注损伤引起的微循环紊乱和细胞需氧代谢破坏。经肝乳酸梯度可作为缺血预适应疗效的监测和预后工具。

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