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猪半肝切除术中长时间持续或间歇性血管流入阻断。

Prolonged continuous or intermittent vascular inflow occlusion during hemihepatectomy in pigs.

作者信息

van Wagensveld B A, van Gulik T M, Gelderblom H C, Scheepers J J, Bosma A, Endert E, Gouma D J

机构信息

Department of Surgery, Academic Medical Center, Amsterdam, The Netherlands.

出版信息

Ann Surg. 1999 Mar;229(3):376-84. doi: 10.1097/00000658-199903000-00011.

DOI:10.1097/00000658-199903000-00011
PMID:10077050
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1191703/
Abstract

OBJECTIVE

To assess ischemia and reperfusion (I/R) injury in a hemihepatectomy model in pigs after prolonged continuous or intermittent vascular inflow occlusion in the liver.

SUMMARY BACKGROUND DATA

Massive intraoperative blood loss during liver resections can be prevented by temporary vascular inflow occlusion, consequently leading to ischemia and reperfusion injury in the remnant liver. Previously, in a pig liver resection model in which only limited I/R injury was induced during brief (90 min) vascular inflow occlusion, the authors demonstrated reduced I/R injury after continuous (CNT) occlusion, compared to intermittent (INT). This liver resection study on pigs was undertaken to assess I/R injury after prolonged (120 min) CNT or INT occlusion.

METHODS

In pigs (37.0 +/- 1.5 kg), liver ischemia during 2 hours was CNT (n = 6) or INT (n = 6) (eight subsequent periods of 12 min ischemia and 3 min recirculation), followed by 6 hours of reperfusion. A left hemihepatectomy (45.5% +/- 1.4%) was performed within the first 12 minutes of ischemia. No hepatic pedicle clamping or liver resection was performed in control experiments (n = 6). Microvascular damage was assessed by hyaluronic acid (HA) uptake capacity of the liver (parameter of early sinusoidal endothelial cell damage) and restoration of intrahepatic tissue pO2 during reperfusion. Hepatocellular damage was tested by plasma concentrations of aspartate aminotransferase (AST), alanine aminotransferase, and lactate dehydrogenase (LDH).

RESULTS

Hyaluronic acid uptake after 6 hours of reperfusion, compared to preischemic uptake, was unaltered in the control group, but was significantly reduced in both resection groups. However, more HA was taken up after INT occlusion, compared to CNT (60.4% +/- 5.6% and 39.5% +/- 3.7%, respectively; ANOVA: p = 0.001). Intrahepatic tissue pO2 distribution after 6 hours of reperfusion more closely returned to preischemic configuration in the INT group than in the CNT group, indicating reduced microcirculatory disturbances after INT occlusion. Release of AST and LDH after 6 hours of reperfusion was significantly increased in both CNT and INT groups. Lower AST levels, however, were found after INT occlusion than after CNT occlusion (267.0 +/- 74.7 U/l and 603.3 +/- 132.4 U/l, respectively; p = 0.06).

CONCLUSIONS

Intermittent hepatic vascular inflow occlusion during prolonged liver ischemia in pigs resulted in less microcirculatory and hepatocellular injury, compared to continuous occlusion. Intermittent clamping is preferable when prolonged periods of vascular inflow occlusion are applied during liver resections.

摘要

目的

评估猪半肝切除模型中,肝脏长时间持续或间歇性血管入流阻断后的缺血再灌注(I/R)损伤。

总结背景数据

肝切除术中大量失血可通过临时血管入流阻断来预防,这会导致残余肝脏发生缺血再灌注损伤。此前,在一个猪肝切除模型中,短暂(90分钟)血管入流阻断期间仅诱导了有限的I/R损伤,作者发现与间歇性(INT)阻断相比,持续(CNT)阻断后I/R损伤减轻。本项关于猪的肝切除研究旨在评估长时间(120分钟)CNT或INT阻断后的I/R损伤。

方法

在猪(37.0±1.5千克)中,进行2小时的肝脏缺血,采用CNT(n = 6)或INT(n = 6)(随后八期,每期缺血12分钟,再灌注3分钟),然后再灌注6小时。在缺血的前12分钟内进行左半肝切除(45.5%±1.4%)。对照实验(n = 6)中不进行肝蒂夹闭或肝切除。通过肝脏透明质酸(HA)摄取能力(早期肝窦内皮细胞损伤参数)和再灌注期间肝内组织pO2的恢复来评估微血管损伤。通过血浆中天冬氨酸转氨酶(AST)、丙氨酸转氨酶和乳酸脱氢酶(LDH)的浓度检测肝细胞损伤。

结果

与缺血前摄取相比,再灌注6小时后对照组的HA摄取未改变,但两个切除组均显著降低。然而,与CNT相比,INT阻断后摄取的HA更多(分别为60.4%±5.6%和39.5%±3.7%;方差分析:p = 0.001)。再灌注6小时后,INT组肝内组织pO2分布比CNT组更接近缺血前状态,表明INT阻断后微循环紊乱减轻。CNT组和INT组再灌注6小时后AST和LDH的释放均显著增加。然而,INT阻断后AST水平低于CNT阻断后(分别为267.0±74.7 U/l和603.3±132.4 U/l;p = 0.06)。

结论

与持续阻断相比,猪长时间肝脏缺血期间间歇性肝血管入流阻断导致的微循环和肝细胞损伤更少。肝切除术中应用长时间血管入流阻断时,间歇性夹闭更可取。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6af/1191703/ee00ff2afa7d/annsurg00003-0097-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6af/1191703/ee00ff2afa7d/annsurg00003-0097-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a6af/1191703/ee00ff2afa7d/annsurg00003-0097-a.jpg

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