Studies on the site of the block in gluconeogenesis causing severe hypoglycemia in intestinal ischemia shock in rats.

Intestinal ischemia shock was induced by 35 to 40-min portal vein occlusion (PVO). After treatment with rat plasma a severe hypoglycemia ensues which is caused by a block in gluconeogenesis. This hypoglycemia is not affected by treatment with adrenaline, glucagon, nicotinadenine dinucleotide (NAD), adenosine triphosphate (ATP) alanine (A), or pyruvate (P), while fructose (F) and dihydroxyacetone (DHA) slightly increase the plasma glucose concentration. If F or DHA are combined with NAD a considerable hyperglycemic effect is observed, but NAD plus A or P is ineffective. A similar marked rise in plasma glucose is observed if F is combined with nicotinamide, adenylic acid, or histamine. NAD causes vasodilatation in the splanchnic area and an increased portal flow. It is concluded that the effect of NAD is the result of an increased uptake of suitable substrates of gluconeogenesis from the peritoneal cavity and/or an increased availability of these substrates to the liver. During the development of PVO shock, portal venous flow diminishes considerably. This reduced flow may be the result of vasoconstriction caused by the high level of plasma adrenaline.