Hyperglycemia, Polyol Accumulation, and Increased Intracranial Pressure

Prockop, Leon D.

doi:10.1001/archneur.1971.00490020044005

Cited by 56 publications

(36 citation statements)

References 36 publications

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“…The present study does not support these contentions. The levels of CSF sorbitol present in our hyper glycemic rabbits, 0.1-0.2 mmol/kg H 2 O, are similar to those previously reported in the CSF of hyperglycemic dogs (11,12). However, brain sorbitol levels attained a maximum value of only 0.3 mmol/kg H 2 O; such quantities, although higher than normal, are of virtually no osmotic significance.…”

Section: Discussionsupporting

confidence: 88%

“…When the plasma glucose in hyperglycemic dogs is rapidly lowered by intravenous infu sion of 0.9% NaCl, the CSF pressure increases concomitant with a further increase in CSF sorbitol (11). It has been sug gested that the elevated CSF sorbitol might be secondary to accumulation of osmotically significant quantities of sorbitol in brain (11,12,10). The present study does not support these contentions.…”

Section: Discussioncontrasting

confidence: 80%

“…The identity of the idiogenic solute is only speculative at the present time, although many investigators have suggested that it might consist of glucose metabolites (10)(11)(12)33). Our data does not support such a contention, since after 4 h of hyper glycemia, there was no change in the brain glucose total radioactivity (dpm per millimole glucose) ( Table IV).…”

Section: Discussionmentioning

confidence: 99%

“…The brain water content in the insulintreated animals was significantly greater than that of the peritoneal dialysis group (P < 0.05). Thus, although brain swelling may occur when plasma glucose is rapidly lowered without insulin (11,12), there is no increase in brain solute activity and the swelling is of a lesser magnitude.…”

Section: Discussionmentioning

confidence: 99%

“…Although there have been some studies on the changes which occur in the CSF during rapid lowering of plas ma glucose, alterations in water, electrolyte, and carbohydrate metabolism in brain under these circumstances are largely unknown. Furthermore, in previous experimental work, plasma glucose has been lowered by intravenous hydration rather than with insulin (12), so that any possible effects of insulin on brain have not been studied. It is the purpose of the present investi gation to study the changes which occur in brain and CSF during sustained hyperglycemia, and to elucidate the pathophysiology of cerebral edema which may occur during rapid lowering of plasma glucose.…”

Section: Introductionmentioning

confidence: 99%

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Effects of Hyperglycemia and Rapid Lowering of Plasma Glucose in Normal Rabbits

2000

Journal of the American Society of Nephrology

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with comments by ALLEN I. ARIEFF and RICHARD STERNS Reprinted from J. Clin. Invest. 52:571-583, 1973 abstract To investigate the pathophysiology of cerebral edema occurring during treatment of diabetic coma, the effects of hyperglycemia and rapid lowering of plasma glucose were evaluated in normal rabbits. During 2 h of hyperglycemia (plasma glucose = 61 mM), both brain (cerebral cortex) and muscle initially lost about 10% of water content. After 4 h of hyperglycemia, skeletal muscle water content remained low but that of brain was normal. Brain osmolality (Osm) (343 mosmol/kg H2O) was similar to that of cerebrospinal fluid (CSF) (340 mosmol/kg), but increases in the concentration of Na+, K+, Cl-, glucose, sorbitol, lactate, urea, myoinositol, and amino acids accounted for only about half of this increase. The unidentified solute was designated "idiogenic osmoles". When plasma glucose was rapidly lowered to normal with insulin, there was gross brain edema, increases in brain content of water, Na+, K+, Cl-and idiogenic osmoles, and a signifi cant osmotic gradient from brain (326 mosmol/kg H2O) to plas ma (287 mosmol/kg). By similarly lowering plasma glucose with peritoneal dialysis, increases in brain Na+, K+, C-, and water were significantly less, idiogenic osmoles were not pres ent, and brain and plasma Osm were not different. It is con cluded that during sustained hyperglycemia, the cerebral cortex adapts to extracellular hyperosmolality primarily by accumula tion of idogenic osmoles rather than loss of water or gain in solute. When plasma glucose is rapidly lowered with insulin, an osmotic gradient develops from brain to plasma. Despite the brain to plasma osmotic gradient, there is no net movement of water into brain until plasma glucose has fallen to at least 14 mM, at which time cerebral edema occurs.

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Section: Discussionsupporting

confidence: 88%