Metabolismo da glicose cerebral no trauma crânio-encefálico: uma avaliação

Schelp, AO.; Burini, R.C.

doi:10.1590/S0004-282X1995000400026

Resumos

Os autores apresentam revisão geral da distribuição e metabolização da glicose, com ênfase para os distúrbios que ocorrem no trauma crânio-encefálico, como a hiperglicemia que ocorre na fase aguda. Finalizando, são feitos comentários sobre as possíveis conseqüências desses conhecimentos sobre os procedimentos atuais, que aconselham a restrição na oferta de glicose a pacientes com catabolismo acentuado e que necessitam poupar o contingente de proteína corporal.

glicose; metabolismo cerebral; trauma crânio-encefálico; hiperglicemia

The authors give a general overview on the cerebral glucose metabolism, with special reference to brain injury, including intake, blood-brain barrier properties for glucose transport, oxidative metabolism and energetic needs during the head trauma. The evidences of the presence of ischemia and hypoxia in those situations and the relationships with the cerebral glucose metabolism are discussed. They point to the several explanations for hyperglicemia present up to 10 days after admission in brain injury, relating to the energetic needs at different phases of head trauma recovery. Some considerations are made about the lack of evidences on increase in glucose consumption or lactate production when hyperglycemia occurs in association with brain damage and ischemia caused by head trauma. The brain capacity to compensate metabolic disturbances is discussed. Some questions are made about current indications for restriction of glucose infusion in pacients who are in catabolic phase and need to spare their body protein pool. At the same way, the polemic about previous hyperglycemia and cerebral injury is revised. Some considerations are made about the moment to introduct increases in glucose administration.

glucose; cerebral metabolism; hyperglycemia; head injury

Metabolismo da glicose cerebral no trauma crânio-encefálico. Uma avaliação

Cerebral glucose metabolism and head injury: an overview

AO. Schelp^I; R.C. Burini^II

^IMédico, pós-graduando do Curso de Patologia. Faculdade de Medicina de Botucatu, Universidade Estadual Paulista (UNESP)

^IIProfessor Titular, Departamento de Clínica Médica, Chefe do Laboratório de Bioquímica Nutricional e Metabólica. Faculdade de Medicina de Botucatu, Universidade Estadual Paulista (UNESP)

RESUMO

Os autores apresentam revisão geral da distribuição e metabolização da glicose, com ênfase para os distúrbios que ocorrem no trauma crânio-encefálico, como a hiperglicemia que ocorre na fase aguda. Finalizando, são feitos comentários sobre as possíveis conseqüências desses conhecimentos sobre os procedimentos atuais, que aconselham a restrição na oferta de glicose a pacientes com catabolismo acentuado e que necessitam poupar o contingente de proteína corporal.

Palavras chave: glicose, metabolismo cerebral, trauma crânio-encefálico, hiperglicemia.

SUMMARY

The authors give a general overview on the cerebral glucose metabolism, with special reference to brain injury, including intake, blood-brain barrier properties for glucose transport, oxidative metabolism and energetic needs during the head trauma. The evidences of the presence of ischemia and hypoxia in those situations and the relationships with the cerebral glucose metabolism are discussed. They point to the several explanations for hyperglicemia present up to 10 days after admission in brain injury, relating to the energetic needs at different phases of head trauma recovery. Some considerations are made about the lack of evidences on increase in glucose consumption or lactate production when hyperglycemia occurs in association with brain damage and ischemia caused by head trauma. The brain capacity to compensate metabolic disturbances is discussed. Some questions are made about current indications for restriction of glucose infusion in pacients who are in catabolic phase and need to spare their body protein pool. At the same way, the polemic about previous hyperglycemia and cerebral injury is revised. Some considerations are made about the moment to introduct increases in glucose administration.

Key words:glucose, cerebral metabolism, hyperglycemia, head injury.

Texto completo disponível apenas em PDF.

Full text available only in PDF format.

Aceite: 15-abril-1995.

Dr. Arthur Oscar Schelp - Departamento de Neurologia e Psiquiatria, Faculdade de Medicina, UNESP - 18618-000 Botucatu SP - Brasil.

1. Baker AJ, Moulton RJ, MacMillan VH, Shedden PM. Excitatory amino acids in cerebrospinal fluid following traumatic brain injury in humans. J Neurosurg 1993, 79:369-372.
2. Baron AD, Brechtel G, Wallace P, Edelman SV. Rates and tissue sites of non-insulin and insulin mediated glucose uptake in humans. Am J Physiol 1988, 255:E769-E774.
3. Bell GI, Kayano T, Buse JB et al. Molecular biology of glucose transporter. Diabetes Care 1990, 13:198-208.
4. Bessey PQ, Watters JM, Aoki TT Willmore DW. Combined hormonal infusion simulates the metabolic response to injury. Ann Surg 1984, 200:264-281.
5. Brightman MW, Reese TS. Junctions between intimately apposed cell membranes in the vertebrate brain. J Cell Biol 1969, 40:648-677.
6. Castellino P, Luzi L, Del Prato S, De Fronzo RA. Dissociation of the effects of epinephrine and insulin on glucose and protein metabolism. Am J Physiol 1990, 258:E117-E125.
7. Cuthbertson DP. The metabolic response to injury and its nutricional implications retrospect and prospect. Second Annual Jonathan E. Rhoads Lecture. J Par Ent Nutr 1979, 3:108-112.
8. Deutschman CS, Konstantinides FN, Cerra FB. Hypermetabolim is not persistent in closed-head injury. Crit Care Med 1986, 14:336.
9. Erecinska M, Silver A. Relationship between ions and energy metabolism: cerebral calcium movements during ischemia and subsequent recovery. Can J Physiol Pharmacol 1992, 70:S190-S193.
10. Gjedde A, Hansen AJ, Quistorff B. Blood-brain glucose transport in spreading depression. J Neurochem 1981, 37:807-812.
11. Hansen AJ. Effects of anoxia on ion distribution in the brain. Physiol Rev 1985, 65:101-148.
12. Hargreaves RJ, Planas AM, Cremer JE, Cunningham UJ. Studies of the relationship between cerebral glucose transport and phosphorylation using 2-deoxyglucose. J Cer Blood Flow Metab 1986, 5:708-716.
13. Harik SI, Kalasia RN, Anderson L, Lundahl P, Perry G. Immunocytochemical localization of erythroid glucose transporter: abundance in tissues with barrier functions. J Neurosci 1990, 10:3862-3872.
14. Hawkins RA, Mans AM, Davis DW, Hibband LS, Lu DM. Glucose availability to individual cerebral structures is correlated to glucose metabolism. J Neurochem 1983, 40:1013-1018.
15. Hertz L, Code WE, Sycova E. Ions, water and energy in brain cells: a synopsis of interrelations. Can. J Physiol Pharmacol 1992, 70:S100-S106.
16. Hörtnagl H, Hammerle AF, Hackl JM et al. The activity of the sympathetic nervous system following severe head injury. Intens Care Med 1980, 6:169-177.
17. Howard JM. Studies of the absorption and metabolism of glucose following injury. Ann Surg 1955, 141:321-326.
18. Janzer RC, Raff MC. Astrocytes induce blood-brain barrier properties in endothelial cells. Nature 1987, 325:253-257.
19. Jeevanandam M, Young DH, Schiller WR. Glucose turn-over, oxidation and indices of recicling in severely traumatized patients. J Trauma 1990, 30:582-589.
20. Jeevanandam M, Young DH, Schiller WR. Endogenous protein-synthesis efficiency in trauma victims. Metabolism 1989, 38:967-973.
21. Karnousky MC, Reich P, Anchors JM, Burrows BL. Changes in brain glycogen during slow-wave sleep in the rat. J Neurochem 1983, 41:1498-1501.
22. Kasanichi MA, Pilch PF. Regulation of glucose transporter function. Diabetes Care 1990, 13:219-227.
23. Katayama Y, Becker DP, Tamura T, Houda DA. Massive increases in intracellular potassium and the indiscriminate release of glutamate following concussive brain injury. J Neurosurg 1990, 73:889-900.
24. Katsura Kl, Ekholm A, Siesjö BK. Coupling among changes in energy metabolism, acid-base homeostasis, and ion fluxes in ischemia. Can J Physiol Pharmacol 1992, 70:S170-S175.
25. Kraig RP, Pulsinelli WA, Plum F. Carbonic acid buffer changes during complete brain ischemia. Am J Physiol 1986, 250:R348-R357.
26. Mantych GJ, James DE, Devaskar SU. Jejunal kidney glucose transporter isoform (Glut 5) is expressed in the human blood-brain barrier. Endocrinology 1993, 132:35-40.
27. Mantych GJ, James DE, Chung HD, Devaskar SU. Cellular localization and characterization of glut 3 glucose transporter isoform in human brain. Endocrinology 1992, 13:1270-1278.
28. Nelson KM, Long CL, Bailey R et al. Regulation of glucose kinetics in trauma patients by insulin and glucagon. Metabolism 1992, 41:68-75.
29. Pelligrino DA, Segil LJ, Albrecht RF. Brain glucose utilization and transport and cortical function in chronic vs. acute hypoglycemia. Am J Physiol 1990, 259:E729-E735.
30. Petersen SR, Jeevanandam M, Harrington T. Is the metabolic response to injury different with or without severe head injury? Significance of plasma glutamine levels. J Trauma 1993, 34:653-661.
31. Petroni A, Borghi A, Blasevich M et al. Effects of hypoxia and recovery on brain eicosanoids and carbohydrate metabolites in rat brain cortex. Brain Res 1987, 415:226-232.
32. Raffin CN, Rosenthal M, Busto R, Sick TJ. Glycolisis, oxidative metabolism and brain potassium. J Cer Blood Flow Metab 1992, 12:34-42.
33. Ritchie DG. Interleukin 6 stimulates hepatic glucose release from prelabeled glycogen pools. Am J Physiol 1990, 258:E57-E64.
34. Sieber FE, Traystman RJ. Glucose and the brain. Crit Care Med. 1992, 20:104-114.
35. Siemkowicz E, Hansen AJ. Clinical restitution following cerebral ischemia in hipo, normo-and hyperglycemic rats. Acta Neurol Scand 1978, 58:1- 8.
36. SiesjöBK. Mechanisms of ischemic brain damage. Crit Care Med 1988, 16:954-963.
37. SiesjöBK. Cerebral circulation and metabolism. J Neurosurg 1984, 60:883-908.
38. Sokoloff L. Energy metabolism and effects of energy depletion or exposure to glutamate. Can J Physiol Pharmacol 1992, 70:S107-S112.
39. Sokoloff L. Metabolism of the central nervous system in vivo. In Field J, Magonon HW. (eds). Handbook of physiology. Baltimore: Waverly, 1960, Vol III, Section I, Neurophysiology.
40. Swanson RA. Physiologic coupling of glial glycogen metabolism to neuronal activity in brain. Can J Physiol Pharmacol 1992, 70:S138-S144.
41. Vanucci RC, Vasta F, Vanucci SJ. Cerebral metabolic response of hyperglicemia in immature rats to hypoxia-ischemia. Pediatr Res 1987, 21:524-529.
42. Yarowsky PJ, Ingvar DH. Neuronal activity and energy metabolism. Fed Proc 1981, 40:2353-2362.
43. Zhuang J, Schmoker JD, Shackford SR, Pietropaoli JA. Focal brain injury results in severe cerebral ischemia despite maintenance of cerebral perfusion pressure. J Trauma 1992, 33:83-88
44. Ziegler TR, Gatzen C, Wilmore DW. Strategies for atenuating protein catabolic responses in the critically ill. Annu Rev Med 1994, 45:459-580.

Datas de Publicação

Publicação nesta coleção
20 Dez 2010
Data do Fascículo
Set 1995

This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

[1] 1. Baker AJ, Moulton RJ, MacMillan VH, Shedden PM. Excitatory amino acids in cerebrospinal fluid following traumatic brain injury in humans. J Neurosurg 1993, 79:369-372.

[2] 2. Baron AD, Brechtel G, Wallace P, Edelman SV. Rates and tissue sites of non-insulin and insulin mediated glucose uptake in humans. Am J Physiol 1988, 255:E769-E774.

[3] 3. Bell GI, Kayano T, Buse JB et al. Molecular biology of glucose transporter. Diabetes Care 1990, 13:198-208.

[4] 4. Bessey PQ, Watters JM, Aoki TT Willmore DW. Combined hormonal infusion simulates the metabolic response to injury. Ann Surg 1984, 200:264-281.

[5] 5. Brightman MW, Reese TS. Junctions between intimately apposed cell membranes in the vertebrate brain. J Cell Biol 1969, 40:648-677.

[6] 6. Castellino P, Luzi L, Del Prato S, De Fronzo RA. Dissociation of the effects of epinephrine and insulin on glucose and protein metabolism. Am J Physiol 1990, 258:E117-E125.

[7] 7. Cuthbertson DP. The metabolic response to injury and its nutricional implications retrospect and prospect. Second Annual Jonathan E. Rhoads Lecture. J Par Ent Nutr 1979, 3:108-112.

[8] 8. Deutschman CS, Konstantinides FN, Cerra FB. Hypermetabolim is not persistent in closed-head injury. Crit Care Med 1986, 14:336.

[9] 9. Erecinska M, Silver A. Relationship between ions and energy metabolism: cerebral calcium movements during ischemia and subsequent recovery. Can J Physiol Pharmacol 1992, 70:S190-S193.

[10] 10. Gjedde A, Hansen AJ, Quistorff B. Blood-brain glucose transport in spreading depression. J Neurochem 1981, 37:807-812.

[11] 11. Hansen AJ. Effects of anoxia on ion distribution in the brain. Physiol Rev 1985, 65:101-148.

[12] 12. Hargreaves RJ, Planas AM, Cremer JE, Cunningham UJ. Studies of the relationship between cerebral glucose transport and phosphorylation using 2-deoxyglucose. J Cer Blood Flow Metab 1986, 5:708-716.

[13] 13. Harik SI, Kalasia RN, Anderson L, Lundahl P, Perry G. Immunocytochemical localization of erythroid glucose transporter: abundance in tissues with barrier functions. J Neurosci 1990, 10:3862-3872.

[14] 14. Hawkins RA, Mans AM, Davis DW, Hibband LS, Lu DM. Glucose availability to individual cerebral structures is correlated to glucose metabolism. J Neurochem 1983, 40:1013-1018.

[15] 15. Hertz L, Code WE, Sycova E. Ions, water and energy in brain cells: a synopsis of interrelations. Can. J Physiol Pharmacol 1992, 70:S100-S106.

[16] 16. Hörtnagl H, Hammerle AF, Hackl JM et al. The activity of the sympathetic nervous system following severe head injury. Intens Care Med 1980, 6:169-177.

[17] 17. Howard JM. Studies of the absorption and metabolism of glucose following injury. Ann Surg 1955, 141:321-326.

[18] 18. Janzer RC, Raff MC. Astrocytes induce blood-brain barrier properties in endothelial cells. Nature 1987, 325:253-257.

[19] 19. Jeevanandam M, Young DH, Schiller WR. Glucose turn-over, oxidation and indices of recicling in severely traumatized patients. J Trauma 1990, 30:582-589.

[20] 20. Jeevanandam M, Young DH, Schiller WR. Endogenous protein-synthesis efficiency in trauma victims. Metabolism 1989, 38:967-973.

[21] 21. Karnousky MC, Reich P, Anchors JM, Burrows BL. Changes in brain glycogen during slow-wave sleep in the rat. J Neurochem 1983, 41:1498-1501.

[22] 22. Kasanichi MA, Pilch PF. Regulation of glucose transporter function. Diabetes Care 1990, 13:219-227.

[23] 23. Katayama Y, Becker DP, Tamura T, Houda DA. Massive increases in intracellular potassium and the indiscriminate release of glutamate following concussive brain injury. J Neurosurg 1990, 73:889-900.

[24] 24. Katsura Kl, Ekholm A, Siesjö BK. Coupling among changes in energy metabolism, acid-base homeostasis, and ion fluxes in ischemia. Can J Physiol Pharmacol 1992, 70:S170-S175.

[25] 25. Kraig RP, Pulsinelli WA, Plum F. Carbonic acid buffer changes during complete brain ischemia. Am J Physiol 1986, 250:R348-R357.

[26] 26. Mantych GJ, James DE, Devaskar SU. Jejunal kidney glucose transporter isoform (Glut 5) is expressed in the human blood-brain barrier. Endocrinology 1993, 132:35-40.

[27] 27. Mantych GJ, James DE, Chung HD, Devaskar SU. Cellular localization and characterization of glut 3 glucose transporter isoform in human brain. Endocrinology 1992, 13:1270-1278.

[28] 28. Nelson KM, Long CL, Bailey R et al. Regulation of glucose kinetics in trauma patients by insulin and glucagon. Metabolism 1992, 41:68-75.

[29] 29. Pelligrino DA, Segil LJ, Albrecht RF. Brain glucose utilization and transport and cortical function in chronic vs. acute hypoglycemia. Am J Physiol 1990, 259:E729-E735.

[30] 30. Petersen SR, Jeevanandam M, Harrington T. Is the metabolic response to injury different with or without severe head injury? Significance of plasma glutamine levels. J Trauma 1993, 34:653-661.

[31] 31. Petroni A, Borghi A, Blasevich M et al. Effects of hypoxia and recovery on brain eicosanoids and carbohydrate metabolites in rat brain cortex. Brain Res 1987, 415:226-232.

[32] 32. Raffin CN, Rosenthal M, Busto R, Sick TJ. Glycolisis, oxidative metabolism and brain potassium. J Cer Blood Flow Metab 1992, 12:34-42.

[33] 33. Ritchie DG. Interleukin 6 stimulates hepatic glucose release from prelabeled glycogen pools. Am J Physiol 1990, 258:E57-E64.

[34] 34. Sieber FE, Traystman RJ. Glucose and the brain. Crit Care Med. 1992, 20:104-114.

[35] 35. Siemkowicz E, Hansen AJ. Clinical restitution following cerebral ischemia in hipo, normo-and hyperglycemic rats. Acta Neurol Scand 1978, 58:1- 8.

[36] 36. SiesjöBK. Mechanisms of ischemic brain damage. Crit Care Med 1988, 16:954-963.

[37] 37. SiesjöBK. Cerebral circulation and metabolism. J Neurosurg 1984, 60:883-908.

[38] 38. Sokoloff L. Energy metabolism and effects of energy depletion or exposure to glutamate. Can J Physiol Pharmacol 1992, 70:S107-S112.

[39] 39. Sokoloff L. Metabolism of the central nervous system in vivo. In Field J, Magonon HW. (eds). Handbook of physiology. Baltimore: Waverly, 1960, Vol III, Section I, Neurophysiology.

[40] 40. Swanson RA. Physiologic coupling of glial glycogen metabolism to neuronal activity in brain. Can J Physiol Pharmacol 1992, 70:S138-S144.

[41] 41. Vanucci RC, Vasta F, Vanucci SJ. Cerebral metabolic response of hyperglicemia in immature rats to hypoxia-ischemia. Pediatr Res 1987, 21:524-529.

[42] 42. Yarowsky PJ, Ingvar DH. Neuronal activity and energy metabolism. Fed Proc 1981, 40:2353-2362.

[43] 43. Zhuang J, Schmoker JD, Shackford SR, Pietropaoli JA. Focal brain injury results in severe cerebral ischemia despite maintenance of cerebral perfusion pressure. J Trauma 1992, 33:83-88

[44] 44. Ziegler TR, Gatzen C, Wilmore DW. Strategies for atenuating protein catabolic responses in the critically ill. Annu Rev Med 1994, 45:459-580.