Partial Portal Vein Arterialization Attenuates Acute Bile Duct Injury Induced by Hepatic Dearterialization in a Rat Model

Hepatic infarcts or abscesses occur after hepatic artery interruption. We explored the mechanisms of hepatic deprivation-induced acute liver injury and determine whether partial portal vein arterialization attenuated this injury in rats. Male Sprague-Dawley rats underwent either complete hepatic arterial deprivation or partial portal vein arterialization, or both. Hepatic ischemia was evaluated using biochemical analysis, light microscopy, and transmission electron microscopy. Hepatic ATP levels, the expression of hypoxia- and inflammation-associated genes and proteins, and the expression of bile transporter genes were assessed. Complete dearterialization of the liver induced acute liver injury, as evidenced by the histological changes, significantly increased serum biochemical markers, decreased ATP content, increased expression of hypoxia- and inflammation-associated genes and proteins, and decreased expression of bile transporter genes. These detrimental changes were extenuated but not fully reversed by partial portal vein arterialization, which also attenuated ductular reaction and fibrosis in completely dearterialized rat livers. Collectively, complete hepatic deprivation causes severe liver injury, including bile infarcts and biloma formation. Partial portal vein arterialization seems to protect against acute ischemia-hypoxia-induced liver injury.

Development of Collaterals in Intermittent and Permanent Ischemia of the Liver

The ischemia caused by hepatic dearterialization as therapy for hepatic malignancies is transient because of the rapid formation of collaterals. In order to prevent this transient repeated ischemia has been suggested.An experimental study was planned to compare the collateral occurrence in persistent ischemia and transient repeated ischeamia of the liver. Fourteen dogs (seven persistent ischemia, seven transient repeated ischemia) were used in this study. Hepatic dearterialization were performed in both groups. In the first group (persistent ischemia), the hepatic artery was ligated proximal to the gastroduodenal artery. In the second group (transient repeated ischemia), the hepatic artery was occluded externally in the same region as the first group by means of a device modified from 8 guage Foley catheter and after occlusion for one hour it was reopened. Occlusions were repeated twice in a day. Five dogs in the first group and six dogs in the second group completed a three weeks ischemia period and angiography were then performed in all. The dogs were sacrificed after the angiography and examined for possible abscess formation, arterial thrombosis, peritoneal adhesions and liver necrosis. After angiography, the two groups were also examined for collateral occurrence. Only one collateral occurred in the transient repeated ischemia group, but in the persistent ischemia group, collaterals occurred in all dogs. This difference between two groups is statistically significant (Fischer Absolute Chi Square Test, p=0.013).Transient repeated ischemia is superior to persistent ischemia because of fewer collaterals, but in practise, total dearterialization of the liver is impossible.

Repeated Hepatic Dearterialization for Unresectable Liver Metastases From Gastric Cancer: Review of Five Cases

A novel method of repeated hepatic dearterialization was evaluated in five patients with multiple metastases from gastric cancer in both hepatic lobes. After gastrectomy with extensive lymph node dissection (R2/3), all patients underwent implantation of a vascular occluder around the hepatic artery. Cannulation of the hepatic artery was added for later chemotherapy. The hepatic artery was occluded repeatedly for 1 hour twice daily in combination with intrahepatic infusion of anticancer drugs for as long as possible. Three of five patients demonstrated marked tumour regression with unexpectedly long survival (16 months in two patients and one still alive at 15 months). Carcinoembryonic antigen (CEA) levels decreased to almost normal in four patients who had initially high levels. The present experiences seems to indicate that long survival can be hoped for in patients with advanced gastric cancer with unresectable liver metastases.