WITH recent attempts to delineate the metabolic alterations responsible for anhepatic coma, it has become apparent that our knowledge of normal as well as pathologic hepatic metabolism is severely inadequate. Previous studies have revealed that hepatic failure following surgical hepatectomy is accompanied by alterations in the tricarboxylic acid cycle such as a rising blood level of α-ketoglutaric acid.1 Citric acid is of general importance in intermediate metabolism due to its presence in this cycle which forms a connecting link between the three main metabolic pathways for the aerobic metabolism of carbohydrate, fat, and protein.2 Boothby and Adams3 have noted increased urinary citrate in anhepatic dogs. Hypercitricemia has been found to accompany pathological liver conditions such as hepatitis and cirrhosis.4 These findings indicate that the liver's role in citrate metabolism merits further investigation.
Extracorporeal perfusion of the isolated liver has been used in studies of hepatic metabolism
VANG JO, ZEMEL R, DAVIDSON M, DRAPANAS T. Citrate Metabolism by the Isolated Perfused Liver. Arch Surg. 1966;93(1):142–147. doi:10.1001/archsurg.1966.01330010144017
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