Contribution of glucose to the hyperosmolality of prolonged hypovolemia.
Normal rats subjected to hypovolemic shock (Wiggers model) exhibited the characteristic rise in blood glucose as well as the initial fall in hematocrit indicative of plasma refill. Concurrently there was a rise in osmolality. Late in shock these animals became hypoglycemic and the hematocrit rose despite a persisting hyperosmolality. Rats which had been deprived of food for 24 hours in order to deplete the liver glycogen did not become hyperglycemic after hemorrhage and had a less marked fall in hematocrit. The plasma osmolality rose to the same high level as that of the fed rats but the rise was slower. From this we conclude that glucose may be largely responsibile for the rise in osmolality early in shock in fed animals but it is not responsible for the continuing hyperosmolality in fed or fasted animals. Nor is it responsible for the initial rise in fasted animals. Hyperosmolality may delay but does not prevent fluid loss from the capillaries late in shock.
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism*; D001835:Body Weight; D005215:Fasting; D006400:Hematocrit; D006943:Hyperglycemia / Q000097:blood; D007022:Hypotension / Q000097:blood; D008297:Male; D009994:Osmolar Concentration; D051381:Rats; D012769:Shock / Q000097:blood*
D001786:Blood Glucose