We analyzed the primary tumors, sonographic findings, clinical manifestations, and prognosis in five cases of isolated splenic metastases to determine in what situations these rare metastases should be suspected. The metastases were detected by ultrasonography in all five patients, and the primary tumors were colonic cancer in four patients and renal cancer in one patient. Splenectomy was performed and the postoperative course was uneventful in all patients. We conclude that preoperative and follow-up examinations must be performed with special attention given to the spleen in colonic or renal cancer patients.

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The objective of this study was to develop an easy and simple experimental rat model of total hepatectomy, hepatic ischemia and extrahepatic portal obstruction. The first operation involved transposing the spleen with its scarified capsule in a subcutaneous pouch to produce portasystemic anastomosis. Total hepatectomy was easily performed in a lobe-by-lobe fashion 2 weeks following the first stage operation. Anhepatic rats receiving a glucose infusion survived for about 10 hours and all died of acute hepatic failure. Hepatic support systems can be accurately evaluated in this anhepatic rat model because of its uniformity. Sixty minutes of hepatic ischemia was able to be performed in rats with a transposed spleen for a portasystemic shunt and no complicated or technically involved procedure was required for the ischemic model. No rats died due to technical difficulties, suggesting the reliability and reproducibility of this ischemic model. An animal model resembling extrahepatic portal vein obstruction was also obtained by ligation of the portal vein; a simple maneuver which was able to produce collateral veins to the liver and cavernous transformation, as similarly seen in clinical patients with extrahepatic portal obstruction. Because these 3 animal models were so easily achieved in the rat, and since the changes in hepatic function and formation of the collaterals to the liver after portal vein occlusion are still poorly understood, this model should prove valuable for future study.

Although it has been firmly established that D-glucose inhibits glucagon secretion from pancreatic A cells, the regulatory mechanism of glucagon secretion by D-glucose has not been elucidated. To study this regulatory mechanism by D-glucose, the effects of hexoses and their derivatives on glucagon secretion from the A cells of isolated perfused rat pancreas were investigated. When these cells were perfused with D-glucose, D-fructose, D-sorbitol, D-galactose, 2-deoxy-D-glucose, D-gluconic acid sodium salt and D-glucosamine HCl salt, glucagon secretion was significantly inhibited. None of the hexoses or their derivatives tested were found to stimulate glucagon secretion. The effects of these sugars on glucagon secretion were independent of their metabolism in the cells. From the findings that the sugars both metabolized and unmetabolized in the cells demonstrated comparable inhibition of glucagon secretion from the isolated perfused rat pancreas, it is speculated that the recognition system for these sugars may be probably present on the A cell membrane and responsible for mediating these inhibitory effects of glucagon secretion.

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