[Formation of portal venous collaterals after ligation of the portal vein for induction of liver regeneration]

TY - JOUR

T1 - [Formation of portal venous collaterals after ligation of the portal vein for induction of liver regeneration]

AU - Krupski, G

AU - Bröring, D C

AU - Wittkugel, Oliver

AU - Müller, L

AU - Nicolas, V

AU - Rogiers, X

AU - Adam, G

AU - Bücheler, E

PY - 2002

Y1 - 2002

N2 - PURPOSE: Unilateral occlusion of the portal vein induces contralateral lobar hypertrophy - in contrast to complete portal vein occlusion which will result in a cavernous transformation. The impact of the formation of collaterals in partial portal vein occlusion is not sufficiently known. The lobar-hypertrophy- phenomenon is in clinical use for several years to induce iatrogenic liver growth to enable extended resections. After portal vein ligation in patients prior to extended hepatic resections, we noticed a perfusion of the formerly occluded side on CT. Using the well-established mini pig model, we were interested whether portal collaterals are formed as cause of the reperfusion. Ex-situ angiograms of the liver were used for the depiction of collaterals. MATERIALS AND METHODS: Using a median laparotomy as access for preparation of the hepatoduodenal ligament, a proximal left portal vein ligation was performed in eight mini pigs under general anesthesia. The total arrest of the portal blood flow (except in segments VI and VII) was documented by duplex ultrasound. After 4 weeks, all pigs were sacrificed and the weight of the ligated liver segments and non-ligated liver segments was measured and compared to a sham group (n = 5). After insertion of a guiding sheath, an ex-situ DSA of the portal vein was acquired. RESULTS: Compared with the sham group, the liver weight increased by 60 % (23 - 99 %, std. dev. 30 %) in segments VI and VII. Atrophy of the ligated segments was signified by a weight loss of 10 % (standard deviation 15 %). The ex-situ angiograms revealed a uniform pattern of collaterals with subsequent complete total recanalization of the formerly occluded portal vein distal from the ligation. The collaterals reduced the portal venous flow rate. CONCLUSION: After portal vein ligation, uniform collateralization results in recanalization of the occluded portal vein. The extent of the collaterals exceeds the known cavernous transformation. The increase in liver volume is not restrained by the formation of collaterals.

AB - PURPOSE: Unilateral occlusion of the portal vein induces contralateral lobar hypertrophy - in contrast to complete portal vein occlusion which will result in a cavernous transformation. The impact of the formation of collaterals in partial portal vein occlusion is not sufficiently known. The lobar-hypertrophy- phenomenon is in clinical use for several years to induce iatrogenic liver growth to enable extended resections. After portal vein ligation in patients prior to extended hepatic resections, we noticed a perfusion of the formerly occluded side on CT. Using the well-established mini pig model, we were interested whether portal collaterals are formed as cause of the reperfusion. Ex-situ angiograms of the liver were used for the depiction of collaterals. MATERIALS AND METHODS: Using a median laparotomy as access for preparation of the hepatoduodenal ligament, a proximal left portal vein ligation was performed in eight mini pigs under general anesthesia. The total arrest of the portal blood flow (except in segments VI and VII) was documented by duplex ultrasound. After 4 weeks, all pigs were sacrificed and the weight of the ligated liver segments and non-ligated liver segments was measured and compared to a sham group (n = 5). After insertion of a guiding sheath, an ex-situ DSA of the portal vein was acquired. RESULTS: Compared with the sham group, the liver weight increased by 60 % (23 - 99 %, std. dev. 30 %) in segments VI and VII. Atrophy of the ligated segments was signified by a weight loss of 10 % (standard deviation 15 %). The ex-situ angiograms revealed a uniform pattern of collaterals with subsequent complete total recanalization of the formerly occluded portal vein distal from the ligation. The collaterals reduced the portal venous flow rate. CONCLUSION: After portal vein ligation, uniform collateralization results in recanalization of the occluded portal vein. The extent of the collaterals exceeds the known cavernous transformation. The increase in liver volume is not restrained by the formation of collaterals.

M3 - SCORING: Zeitschriftenaufsatz

VL - 174

SP - 1281

EP - 1284

JO - ROFO-FORTSCHR RONTG

JF - ROFO-FORTSCHR RONTG

SN - 1438-9029

IS - 10

M1 - 10

ER -