Continuous or intermittent vascular clamping during hemihepatectomy in pigs: hyaluronic acid kinetics in the assessment of early microvascular liver damage.

B A van Wagensveld, T M van Gulik, H C Gelderblom, J J Scheepers, A Bosma, E Endert, H Obertop, D J Gouma
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引用次数: 20

Abstract

Objective: To assess the uptake of hyaluronic acid (HA) as a marker of microvascular damage in a model of hemihepatectomy in pigs having continuous or intermittent vascular inflow occlusion.

Design: Prospective, animal study.

Setting: Laboratory for experimental surgery, University hospital, The Netherlands.

Interventions: Total liver ischaemia was achieved during 90 minutes by continuous (n = 5) or intermittent (n = 5) occlusion of the portal vein and hepatic artery followed by 120 minutes of reperfusion. In a second series of pigs (n = 8) a left hemihepatectomy was added to the protocol.

Main outcome measures: Uptake of exogenous HA was assessed before ischaemia and after 120 minutes of reperfusion, together with the galactose elimination capacity. Plasma activities of aspartate aminotransferase (AST), alanine amino transferase, and lactate dehydrogenase were measured and specimens of liver were obtained for histopathological examination.

Results: HA uptake was slightly reduced after reperfusion in unresected livers compared with uptake before ischaemia. After hemihepatectomy HA uptake after reperfusion was significantly reduced after both continuous and intermittent occlusion, but more HA was taken up after continuous occlusion (p = 0.02). Release of AST after reperfusion was increased only after hemihepatectomy.

Conclusions: Microvascular damage, as assessed by HA uptake capacity, significantly contributed to normothermic ischaemia and reperfusion injury in porcine liver. Vascular inflow occlusion during 90 minutes in combination with hemihepatectomy resulted in less liver damage when vascular occlusion was continuous rather than intermittent.

猪半肝切除术期间连续或间歇血管夹持:透明质酸动力学在早期微血管肝损伤评估中的应用。
目的:评估连续或间歇血管流入阻塞猪半肝切除模型中透明质酸(HA)的摄取作为微血管损伤的标志。设计:前瞻性动物研究。地点:荷兰大学医院实验外科实验室。干预措施:通过连续(n = 5)或间歇(n = 5)阻断门静脉和肝动脉,在90分钟内实现全肝缺血,然后再灌注120分钟。在第二组猪(n = 8)中,在方案中增加了左半肝切除术。主要结局指标:在缺血前和再灌注120分钟后评估外源性HA的摄取,以及半乳糖消除能力。测定血浆中谷草转氨酶(AST)、丙氨酸氨基转移酶(alanine氨基转移酶)和乳酸脱氢酶(乳酸脱氢酶)的活性,并取肝脏标本进行组织病理学检查。结果:与缺血前相比,未切除肝脏再灌注后HA摄取略有减少。半肝切除术后,连续和间歇阻断后再灌注后HA摄取均显著降低,但连续阻断后HA摄取更多(p = 0.02)。再灌注后AST释放仅在半肝切除术后增加。结论:通过HA摄取能力评估,微血管损伤是猪肝缺血再灌注损伤的重要原因。血管流入阻断90分钟联合半肝切除术,当血管阻断是连续的而不是间歇性的时,肝损害较小。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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