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Mechanisms of seizures and coma in hypoglycemia. Evidence for a direct effect of insulin on electrolyte transport in brain.
J Clin Invest. 1974 Sep; 54(3):654-63.JCI

Abstract

The mechanisms involved in the production of hypoglycemic coma were studied in rabbits. Measurements were made in brain, cerebrospinal fluid (CSF), and plasma of osmolality, Na(+), K(+), Cl(-), water content, exogenous insulin, glucose, lactate, and glutamate, while pH, Pco(2), Po(2), and bicarbonate were evaluated in arterial blood, 35 min after i.v. injection of insulin (50 U/kg), plasma glucose did not change, but brain K(+) content increased significantly. Grand mal seizures were observed in unanesthetized animals (+/-SD) 133+/-37 min after administration of insulin, at a time when brain glucose was normal, but brain tissue content of Na(+), K(+), osmoles, and water was significantly greater than normal. Coma supervened 212+/-54 min after insulin injection, at which time brain glucose, lactate, and glutamate were significantly decreased. At both 35 and 146 min after insulin administration, exogenous insulin was present in brain, but not in the CSF. After 208 min of insulin administration, animals were given i.v. glucose and sacrificed 35 min later. Most changes in the brain produced by hypoglycemia were reversed by the administration of glucose. Hypoxia (Po(2) = 23 mm Hg) was produced and maintained for 35 min in another group of animals. Hypoxia caused brain edema but did not affect brain electrolyte content. However, brain lactate concentration was significantly greater than normal. The data indicate that the seizures noted early in the course of insulin-induced hypoglycemia are temporally related to a rise in brain osmolality secondary to an increased net transport into brain of Na(+) and K(+), probably caused by insulin, per se. As hypoglycemia persists, there is also depletion of energy-supplying substrates (glucose, lactate, glutamate) in the brain, an event which coincides with the onset of coma. The brain edema observed during hypoxia is largely due to an increase in brain osmolality secondary to accumulation of lactate.

Authors

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Pub Type(s)

Journal Article

Language

eng

PubMed ID

4853137

Citation

Arieff, A I., et al. "Mechanisms of Seizures and Coma in Hypoglycemia. Evidence for a Direct Effect of Insulin On Electrolyte Transport in Brain." The Journal of Clinical Investigation, vol. 54, no. 3, 1974, pp. 654-63.
Arieff AI, Doerner T, Zelig H, et al. Mechanisms of seizures and coma in hypoglycemia. Evidence for a direct effect of insulin on electrolyte transport in brain. J Clin Invest. 1974;54(3):654-63.
Arieff, A. I., Doerner, T., Zelig, H., & Massry, S. G. (1974). Mechanisms of seizures and coma in hypoglycemia. Evidence for a direct effect of insulin on electrolyte transport in brain. The Journal of Clinical Investigation, 54(3), 654-63.
Arieff AI, et al. Mechanisms of Seizures and Coma in Hypoglycemia. Evidence for a Direct Effect of Insulin On Electrolyte Transport in Brain. J Clin Invest. 1974;54(3):654-63. PubMed PMID: 4853137.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Mechanisms of seizures and coma in hypoglycemia. Evidence for a direct effect of insulin on electrolyte transport in brain. AU - Arieff,A I, AU - Doerner,T, AU - Zelig,H, AU - Massry,S G, PY - 1974/9/1/pubmed PY - 1974/9/1/medline PY - 1974/9/1/entrez SP - 654 EP - 63 JF - The Journal of clinical investigation JO - J Clin Invest VL - 54 IS - 3 N2 - The mechanisms involved in the production of hypoglycemic coma were studied in rabbits. Measurements were made in brain, cerebrospinal fluid (CSF), and plasma of osmolality, Na(+), K(+), Cl(-), water content, exogenous insulin, glucose, lactate, and glutamate, while pH, Pco(2), Po(2), and bicarbonate were evaluated in arterial blood, 35 min after i.v. injection of insulin (50 U/kg), plasma glucose did not change, but brain K(+) content increased significantly. Grand mal seizures were observed in unanesthetized animals (+/-SD) 133+/-37 min after administration of insulin, at a time when brain glucose was normal, but brain tissue content of Na(+), K(+), osmoles, and water was significantly greater than normal. Coma supervened 212+/-54 min after insulin injection, at which time brain glucose, lactate, and glutamate were significantly decreased. At both 35 and 146 min after insulin administration, exogenous insulin was present in brain, but not in the CSF. After 208 min of insulin administration, animals were given i.v. glucose and sacrificed 35 min later. Most changes in the brain produced by hypoglycemia were reversed by the administration of glucose. Hypoxia (Po(2) = 23 mm Hg) was produced and maintained for 35 min in another group of animals. Hypoxia caused brain edema but did not affect brain electrolyte content. However, brain lactate concentration was significantly greater than normal. The data indicate that the seizures noted early in the course of insulin-induced hypoglycemia are temporally related to a rise in brain osmolality secondary to an increased net transport into brain of Na(+) and K(+), probably caused by insulin, per se. As hypoglycemia persists, there is also depletion of energy-supplying substrates (glucose, lactate, glutamate) in the brain, an event which coincides with the onset of coma. The brain edema observed during hypoxia is largely due to an increase in brain osmolality secondary to accumulation of lactate. SN - 0021-9738 UR - https://www.unboundmedicine.com/medline/citation/4853137/Mechanisms_of_seizures_and_coma_in_hypoglycemia__Evidence_for_a_direct_effect_of_insulin_on_electrolyte_transport_in_brain_ DB - PRIME DP - Unbound Medicine ER -