The ECK fistula in animals and humans

Augmenter of liver regeneration: Its place in the universe of hepatic growth factors

“…The Eck fistula liver after portacaval shunt was thought -until about 30 yr agoto function normally except for hyperammonemia. This view was inconsistent with the striking hepatocyte atrophy (to half size), deglyogenation and fatty infiltration caused by the operation in all species studied, including human beings (31)(32)(33)(34). At the same time, there is a tripling of liver cell renewal (11,34,35).…”

“…In dogs, both the atrophic and hyperplastic alterations are complete within 4 days and remain stable thereafter ( Table 2). The ultrastructure of the hepatocytes shows a striking disruption of the rough endoplasmic reticulum and depletion of the ribosomes (12,(31)(32)(33)(34)(35)(36)(37)(38), explaining a reduced synthesis of cholesterol and other lipid moieties, bile acids, urea and, presumably, essentially all metabolites of hepatic origin (summarized in reference 33). Lowered activity of the hepatic microsomal mixed function enzyme system for which multiple cytochrome P-450 and P-448 species serve as terminal oxidases account for other subtle but cumulatively massive degradations in hepatic function (33).…”

The mother lode of liver transplantation, with particular reference to our new journal

“…22 Until this time, most surgeons and hepatologists had assumed that the normal human liver functioned essentially normally after portacaval shunting except for hyperammonemia. 23,24 This view was inconsistent with the striking hepatocyte atrophy (to half size), deglycogenation, and fatty infiltration demonstrated in both Eck fistula and double liver models during the 1960s and 1970s 4,12,20 in all species studied, including baboons 25 and humans. 4,26 At the same time, there is a tripling of liver cell renewal.…”

“…10 These previously enigmatic syndromes became comprehensible when insulin finally was proved in 1975 to be the most important hepatotrophic factor in splanchnic venous blood. 4,11,12 Until then, the entrenched dogma of hepatic physiology had been that the volume rather than the source of portal venous blood flow was the critical factor in hepatic homeostasis and control of liver mass (the flow hypothesis 4 ). Now it was evident that the principal liability of the splanchnic diversion procedures came from their placement of the liver in an insulinoprival state.…”

The Surgical Treatment of Portal Hypertension

“…TIPS was shown to be as effective as surgical shunts in controlling bleeding, particularly with technical advances such as covered stents . The recognition that complete portal diversion of blood led to deleterious hepatic dysfunction spurred Starzl to investigate the mechanism by which deprivation of portal blood caused liver atrophy and fatty infiltration, and the hepatocellular ultrastructural changes of depletion and disruption of the smooth endoplasmic reticulum, reduction of membrane‐bound polyribosomes, diminution of glycogen, and deterioration of the mitochondria . It should come as no surprise that one of the finest reviews of that time on the topic of the Eck fistula and its many surgical variants and complications in animals and humans, considered to be the most authoritative publication since that by Pavlov and his associates in 1893, was authored by none other than Tom Starzl and two talented collaborators—the first, a Chair of Pathology in London, UK, would join him later in Denver, and the other a Chair of Biochemistry in Bari, Italy.…”