Abstract
In the fasting state the hepatic venous glucose concn. always exceeds the simultaneous arterial concn. This circumstance makes possible the estimation of the splanchnic glucose production from the product of the hepatic (splanchnic) blood flow (BSP method) and the hepatic arteriovenous glucose difference. This splanchnic glucose production is the balance between true hepatic glucose production and that glucose utilized by the various viscera drained by the portal vein. It is, therefore, termed the net splanchnic glucose production. The net splanchnic glucose production, at a constant arterial concn. of glucose, must balance and, therefore, approximate the rate of peripheral glucose utilization. In 38 normal controls, the hepatic A-V glucose difference averaged 8.5 mg.% and the net splanchnic glucose production 65 mg./min./ sq. m. of body surface. 45 mg. of this is used by the brain leaving 20 mg./min./sq. m. for use in other locations. The slow intravenous infusion of glucose at rates moderately exceeding the splanchnic glucose production obliterates the hepatic A-V glucose difference. The glucose difference between arterial and portal venous bloods, the latter being estimated from portal collateral blood obtained from patients with cirrhosis, is apparently negligible. The net splanchnic glucose production, then, is close to the true hepatic glucose output. In insulin-treated diabetes mellitus, both the hepatic arteriovenous glucose difference and the net splanchnic glucose production are normal. The splanchnic glucose production is low in Laennec''s cirrhosis of the liver. The hepatic arteriovenous glucose difference is normal in hyper-thyroidism, and the splanchnic glucose output is moderately but not significantly elevated. In congestive heart failure, the hepatic arteriovenous glucose difference is high in correspondence to the decreased hepatic blood flow. The rise in glucose difference is not fully compensatory, however, resulting in a somewhat subnormal splanchnic glucose production.

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