Abstract
Olmsted and Read 1 found that in the decapitate cat there was more glucose in hepatic than in portal blood at a time when glycogen was being deposited in the liver. At the same time Tsai and Yi 2 obtained similar results, and also reported 3 that even during absorption of sugar after its injection into the stomach, the concentration of sugar in portal blood in the decapitate cat falls short of that in hepatic blood. We had at the same time completed a similar investigation of the decapitate cat, and had extended our experiments to the amytalized dog, taking into account the behavior of lactic acid in the blood. The data are as follows.
We injected 0.5 gm. glucose per kilo body weight into the duodenum of 2 decapitate cats, the hepatic artery having been ligated in each. Total reducing substance was estimated by Folin-Wu tungstate precipitation; glucose by Somogyi's zinc precipitation; 0.1 cc. samples were used.
In these 2 preparations, blood taken from the portal vein within half an hour after glucose injection contained more glucose than hepatic blood. But within an hour the situation was reversed (Table I).
In a third preparation, in which the hepatic artery was not tied, there was delay in absorption and more glucose was found in hepatic than in portal blood in every case (Table II).
Three dogs under amytal anesthesia were given a solution containing 10 gm. glucose by subcutaneous injection, the hepatic artery being tied. Total blood sugar was determined by the Folin-Wu method, using 1 cc. samples. Lactic acid was determined by the Friedemann, Cotonio, and Shaffer method. Rose, Giragossintz, and Kirstein 4 found that although fructose caused a great increase in blood lactic acid, glucose brought about little, if any, change in lactic acid in portal blood.
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