Abstract
Increased intracranial pressure reproducibly occurs in hyperglycemic dogs when the blood glucose level is permitted to fall precipitously and they are rehydrated with isotonic saline solutions. Water intoxication, carbon dioxide accumulation, and osmotic and electrolyte differences between the cerebrospinal fluid (CSF) and plasma did not play major roles in the production of the observed increases in CSF pressure. There was a significant rise in CSF and brain concentrations of fructose and sorbitol in response to hyperglycemia, suggesting that the level of blood glucose regulates the rate of sorbitol and fructose synthesis within the central nervous system, and that there was an increased activity of the polyol (glucose/sorbitol/ fructose) pathway. This potential for the production of increased intracranial pressure may be responsible for the fatal acute cerebral edema observed during the treatment of diabetic acidosis.

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