Effects of anoxia on cerebral metabolism and electrolytes in man

Meyer, John S.; Gotoh, Fumio; Ebihara, S; Tomita, Minoru

doi:10.1212/wnl.15.10.892

Cited by 86 publications

(22 citation statements)

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“…(b) Cerebral anoxia secondary to impaired cerebral circulation (42) with breakdown of the "Na pump," causing a loss of K+ and a gain of Na+ and water in brain (4,43). In the present study, brain content of both Na+ and K+ increased; these alterations should not occur with anoxia (43).…”

Section: Treatment With Peritoneal Dialysismentioning

confidence: 50%

Studies on Mechanisms of Cerebral Edema in Diabetic Comas. EFFECTS OF HYPERGLYCEMIA AND RAPID LOWERING OF PLASMA GLUCOSE IN NORMAL RABBITS

Arieff¹,

Kleeman²

1973

J. Clin. Invest.

181

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A B S T R A C T 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 H20) 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 significant osmotic gradient from brain (326 mosmol/ kg H20) to plasma (287 mosmol/kg). By similarly lowering plasma glucose with peritoneal dialysis, increases in brain Na+, K+, Cl-, and water were significantly less, idiogenic osmoles were not present, and brain and plasma Osm were not different. It is concluded that during sustained hyperglycemia, the cerebral cortex adapts to extracellular hyperosmolality This work was presented in part at International Symposium on the

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Section: Treatment With Peritoneal Dialysismentioning

confidence: 50%

Studies on Mechanisms of Cerebral Edema in Diabetic Comas. EFFECTS OF HYPERGLYCEMIA AND RAPID LOWERING OF PLASMA GLUCOSE IN NORMAL RABBITS

Arieff¹,

Kleeman²

1973

J. Clin. Invest.

181

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“…In infants with protein-calorie malnutrition, behavior disorders are said to be associated with a deficit in brain K+ [10]. Also, the normal brain water and electrolyte composition is altered by prolonged asphyxia and acute anoxia [6,17] and by an anoxic-ischemic insult [20]. These findings have led to the present study which examines the combined and separate effects of growth retardation and asphyxia on cerebral electrolytes in the postnatal rat.…”

Section: Introductionmentioning

confidence: 99%

Effects of Growth Retardation and Asphyxia on Brain Electrolytes and on Glycolysis in Developing Rats

1973

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ExtractDuring postnatal brain development in the rat there is a progressive decrease in the Na + /K + ratio, which correlated with increasing activity of Na + -K+-activated ATPase. Undernutrition during intrauterine and early postnatal development (4-6 days) did not alter the Na + /K+ ratio, although there was a deficit in brain weight. However, undernutrition during the suckling period retarded the progressive fall in Na+/K+ ratio and rise in ATPase activity. The altered Na+/K + ratio in these animals did not appear to be caused by change in brain carbohydrate metabolism.Developing rats undernourished until 4-6 days resembled the intrauterine growthretarded human baby as regards deficits in body weight, relative sparing of the brain compared with other organs, and depleted carbohydrate reserves.The undernourished 4-6-day-old rat tolerated asphyxia as well as the well nourished rat of the same age. After asphyxia, the Na+/K+ ratio reverted to unity and there was an increase in brain water. Liver carbohydrate reserves did not appear to be a limiting factor that determined the point of death. Speculation

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“…In the pre sent study, brain content of both Na+ and K+ increased; these alterations should not occur with anoxia (43).…”

Section: Discussionmentioning

confidence: 75%

“…(b) Cerebral anoxia secondary to impaired cerebral circula tion (42) with breakdown of the "Na pump," causing a loss of K+ and a gain of Na+ and water in brain (4,43). In the pre sent study, brain content of both Na+ and K+ increased; these alterations should not occur with anoxia (43).…”

Section: Discussionmentioning

confidence: 99%

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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Effects of anoxia on cerebral metabolism and electrolytes in man

Cited by 86 publications

References 0 publications

Studies on Mechanisms of Cerebral Edema in Diabetic Comas. EFFECTS OF HYPERGLYCEMIA AND RAPID LOWERING OF PLASMA GLUCOSE IN NORMAL RABBITS

Studies on Mechanisms of Cerebral Edema in Diabetic Comas. EFFECTS OF HYPERGLYCEMIA AND RAPID LOWERING OF PLASMA GLUCOSE IN NORMAL RABBITS

Effects of Growth Retardation and Asphyxia on Brain Electrolytes and on Glycolysis in Developing Rats

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

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