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ANNALS OF SURGERY
卷 247, 期 5, 页码 825-834出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/SLA.0b013e31816a9d7c
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Background Data: The extent of hepatectomies is limited by the functional reserve of the remnant liver. The introduction of preoperative portal vein occlusion techniques to induce a preoperative hyperplasia of the future liver remnant has reduced the risk of postoperative liver failure. However, it has remained a matter of debate whether partial portal vein embolization (PVE) or suture ligation of the portal branches during exploration is the preferred technique. We compared both techniques under standardized experimental conditions in a large animal model by means of effectiveness and pathophysiologic differences. Methods: Thirteen mini-pigs underwent portal vein ligation (PVL), 11 mini-pigs underwent PVE of 75% of the liver volume, and 6 underwent a sham operation. The animals were killed after 28 days. Laboratory liver function and damage parameters, lobar liver-to-body weight indices, portal and arterial flow alterations, and histologic changes were assessed. Ex situ arteriograms and portograms were performed to examine adaptive changes in the macroarchitecture of both vascular systems. Results: The liver-to-body weight index of the nonoccluded lobe was highest after PVE (0.85) versus 0.6 (P < 0.05) after PVL. There was no significant reduction in global serum parameters reflecting total liver function. After 4 weeks, the PVL group consistently exhibited hepatopetal portal flow in the ligated lobes, which was present but significantly decreased after PVE. The ex situ angiography after PVE and PVL revealed the development of portal neocollaterals in the portal-occluded liver parts. Conclusions: Both PVL and PVE are able to induce hypertrophy of the future liver remnant. In comparison, PVE is the more effective technique to increase the future liver remnant. This is due to a more effective, durable occlusion of the portal branches. Formation of collaterals between occluded and nonoccluded liver parts seems to be the cause of inferior regeneration in the ligation group.
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