The phenomenon of ketosis has interested investigators and clinicians for many years. With the recent rapid strides in the understanding of fat metabolism and the central role of acetyl-CoA in intermediary metabolism (1-5), this subject has taken on added interest. Although it has long been recognized that the liver is the chief site of origin of the ketone bodies, the basis for this has only recently been clarified. Apparently, most tissues are capable of forming acetoacetyl-CoA during the normal course of fatty acid catabolism or by condensation of two molecules of acetylCoA, but only the liver both possesses an enzyme, deacylase, which removes CoA from the molecule to release free acetoacetate, and at the same time lacks the acetoacetate activating enzyme which would result in acetoacetate's re-entering the metabolic cycle as acetoacetyl-CoA. Other tissues have some deacylase activity, but their acetoacetate activating enzyme system is so active that little or no free acetoacetate ever escapes from the cell (4). Ketonemia thus represents the balance between the rate of ketone production by the liver, utilization by extra hepatic tissues and excretion by the kidneys. Hepatic ketone production in turn is a function of the relative rates at which acetyl-CoA and acetoacetyl-CoA are formed, as from fat catabolism, and amino acids, and the rate at which acetyl-CoA can be disposed of by oxidation via the Krebs cycle or by reduction and syn-1

Using the BSP extraction technic, the hepatic blood flow of the dog was found to be reduced markedly following a single massive hemorrhage. However, increase in the arterial hepatic venous-oxygen difference compensated for as much as 75% reduction in flow; hence, splanchnic oxygen consumption was maintained under these circumstances. Significant reduction of splanchnic oxygen consumption occurred only during sustained shock when hepatic blood flow was so seriously diminished that high oxygen extraction could not compensate for the lowered oxygen delivery to the liver.

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