Disturbances in the glucose metabolism in intestinal ischemia shock.
Intestinal ischemia shock is obtained in fasted rats by 40-minute splanchnic arterial occlusion (SAO) or by 35-minute portal vein occlusion (PVO). Survival is prolonged by plasma treatment; further prolongation is obtained by additional administration of glucose. After SAO early hyperglycemia is marked. Plasma adrenaline rises steeply after opening of the arteries and remains high, while plasma insulin remains unaltered. The hyperglycemia is abolished by adrenalectomy and section of the major splanchnic nerves (MSN) proximal to the adrenals but not by section of the MSN distal from the adrenals or by vagotomy. It is concluded that the sympathetic nervous system is stimulated by a substance, possibly related to VIP, released from the intestines. After PVO hyperglycemia is less marked. Plasma adrenaline as well as insulin are increased. During late and fatal hypoglycemia after PVO plus plasma treatment, the liver still appears to be functionally intact. It is assumed that gluconeogenesis is reversibly inhibited by as yet unknown factors. The hypoglycemia cannot be abolished by injection of common substrates of gluconeogenesis but the combination fructose plus glucagon plus NAD is highly effective.
D000313:Adrenal Medulla / Q000503:physiopathology; D000315:Adrenalectomy; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism*; D004837:Epinephrine / Q000097:blood; D005260:Female; D005943:Gluconeogenesis; D006943:Hyperglycemia / Q000209:etiology; D007003:Hypoglycemia / Q000209:etiology; D007422:Intestines / Q000098:blood supply*; D007511:Ischemia / Q000097:blood*; D007668:Kidney / Q000378:metabolism; D008099:Liver / Q000503:physiopathology; D011169:Portal Vein / Q000503:physiopathology; D051381:Rats; D012769:Shock / Q000097:blood*; D014660:Vasoactive Intestinal Peptide / Q000502:physiology
D001786:Blood Glucose; D014660:Vasoactive Intestinal Peptide; D004837:Epinephrine