Thirty-five consecutive cases of adenocarcinoma of the ampulla of Vater seen over the past 36 years were reviewed. The introduction of new diagnostic techniques over the course of this study improved the accuracy of preoperative diagnosis but did not lead to earlier diagnosis. The surgical resectability rate was 88%, and 53% of postoperative survivors were free of disease at 5 years. Of the 14 patients with metastases to regional lymph nodes, 27% survived disease-free for 5 years. Surgical mortality was 25% for the entire series but has been reduced to 6.6% over the past decade. Surgical mortality was primarily due to leakage of the pancreaticojejunostomy; the risk of pancreaticojejunostomy leak correlated inversely with the degree of chronic pancreatitis in the pancreatic remnant. In 35% of resected cases, a benign adenomatous component was contained within the cancer of the ampulla of Vater. Cure rates are good for this lesion. The most important factor in maximizing cure rate is careful attention to the technical details of pancreaticojejunostomy in order to minimize surgical mortality. Benign adenomas appear to be a frequent precursor of carcinoma of the ampulla of Vater.

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tween the potential benefits of the liver support device from A large animal model of fulminant hepatic necrosis is hemodetoxification. No animal model has been developed necessary to test the efficacy of artificial liver support with these ideal characteristics. systems. A recent model was developed using D-galactos-D-galactosamine has been found to cause severe hepatocelamine in anesthetized dogs. Because of the difficulties lular necrosis and a clinical picture similar to fulminant viral encountered with prolonged anesthesia, a similar protohepatitis. 4 It has been extensively studied in various animal col was used in 10 unanesthetized dogs. Intravenous inmodels, including rats, mice, rabbits, and dogs. [5][6][7][8][9][10][11][12] Most refusions of D-galactosamine (1.0 to 1.5 gm/kg) did not recently, a model of lethal galactosamine-induced fulminant sult in uniform death of all animals at 72 hours or hepatic necrosis in anesthetized dogs was developed. 3 In this development of hypoglycemia. Severe hepatic necrosis model, the intravenous injection of D-galactosamine, 1 gm/kg was observed in all animals, but residual hepatocyte viabody weight resulted in universal death within 48 hours. bility was evident in some. All animals developed severeThe animals showed biochemical and clinical abnormalities consumption coagulopathy with histological evidence of typical of FHF, and liver histology characteristic of diffuse disseminated intravascular coagulation (DIC) in four. A hepatocellular necrosis. Unfortunately, halothane anesthesia clinical picture characteristic of endotoxic shock was was used throughout the experiments to minimize potential observed in most animals as a terminal event. The presdistress to the animals. Because halothane is metabolized by ence of endotoxin was confirmed in all dogs tested after the liver, is known to cause hepatocellular damage, and 12 hours (7/10). The differences observed between this shares some metabolic pathways with D-galactosamine, the model and the anesthetized model are probably because possibility of potentiation from halothane cannot be exof the toxic synergism between halothane and D-galaccluded. should use a large animal to allow extracorporeal circulation discomfort or pain to the animals were developed. Analgesic and circuits resembling those used in humans, cause near univer-behavioral doses of morphine sulfate and acepromazine were used sal death from acute liver failure, provide a short and predict-whenever required, but the animals were awake during most of the able time from insult to animal demise, mimic the clinical experiments. picture of acute liver failure, offer a potential for reversibility, Mongrel dogs of either sex weighing 28 to 35 kg were used. The have minimal effect on other organ systems, and be safe for animals were received, given complete physical examinations including complete blood count and blood chemistries, and then conditioned the environment and personnel. 1,3 Furthermore, if a chemical for 6 weeks before initiation of the experiments. ...

These results demonstrate that the microenvironment existing within the surgically repositioned intra-abdominal testis supports the survival of xenogeneic tissue. The survival of xenogeneic tissue in the absence of immunosuppression in this large-animal model raises the possibility that xenogeneic porcine islet tissue will also survive in humans if transplanted into a similar environment.

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