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Structural Aspects of Energy Failure States in the Brain

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Brain Protection

Abstract

The energy produced in the brain is used for three general purposes. First, it is used to support transmission of electrical impulses, including events involved in synaptic activity. This work encompasses both the constant repumping of ions that conduct the currents during nervous activity and the synthesis of neurotransmitters and neuromodulators. This obviously requires a great proportion of the energy produced, but transmission is evidently not a vital function for the nerve cell itself. Thus, with marginal degrees of energy failure (e.g. due to hypoxia, ischemia or hypoglycemia), the neuron may become electrically silent and yet recover completely, if an adequate energy state is restored (see Astrup in this book). The structural detection of cellular injury necessitates visible changes, such as altered form, relationships or stainability of cells. It may be assumed with great confidence (though direct evidence is lacking) that the neurons passing the threshold of “transmission failure” do not show any structural alterations.

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References

  1. Agardh O-D, Kalimo H, Olsson Y, Siesjö BK (1980) Hypoglycemic brain injury. I. Metabolic and light microscopic findings in rat cerebral cortex during profound insulin-induced hypoglycemia and in the recovery period following glucose administration. Acta Neuropathol 50:31–41

    Article  PubMed  CAS  Google Scholar 

  2. Arsenio-Nunes ML, Hossmann KA, Farkas-Bargerton E (1973) Ultrastructural and histochemical investigation of the cerebral cortex of cat during and after complete ischemia. Acta Neuropathol 26:329–344

    Article  PubMed  CAS  Google Scholar 

  3. Astrup J (1982) Energy-requiring cell functions in the ischemic brain. Their critical supply and possible inhibition in protective therapy. J Neurosurg 56:482–497

    Article  PubMed  CAS  Google Scholar 

  4. Brierley JB (1976) Cerebral hypoxia. In: Blackwood W, Corsellis JAN. Eds. Greenfield’s Neuropathology. Edward Arnold, pp 43–85

    Google Scholar 

  5. Brown AW, Brierley JB (1972) Anoxic-ischaemic cell change in rat brain. Light microscopic and fine structural observations. J Neurol Sci 16:59–84

    Article  PubMed  CAS  Google Scholar 

  6. Garcia JH, Kamijyo Y, Kalimo H, Tanaka J, Viloria JE, Trump BF (1975) Cerebral ischemia: The early structural changes and correlation of these with known metabolic and dynamic abnormalities. In: Whisnant JP, Sandok B. Eds. Cerebral vascular diseases. Grune & Stratton, pp 313–323

    Google Scholar 

  7. Garcia JH, Kalimo H, Kamijyo Y, Trump BF (1977) Cellular events during partial cerebral ischemia. I. Electron microscopy of feline cerebral cortex after middle-cerebral artery occlusion. Virchows Arch Cell Pathol 25:191–206

    CAS  Google Scholar 

  8. Ito U, Spatz M, Walker JT jr, Klatzo I (1975) Experimental cerebral ischemia in Mongolian gerbils. Acta Neuropathol 32:209–223

    Article  PubMed  CAS  Google Scholar 

  9. Jenkins LW, Povlishock JT, Becker DP, Miller JD, Sullivan HG (1979) Complete cerebral ischemia. An ultrastructural study. Acta Neuropathol 48:113–125

    Article  PubMed  CAS  Google Scholar 

  10. Jenkins LW, Povlishock JT, Lewelt W, Miller JD, Becker DP (1981) The role of postischemic recirculation in the development of ischemic neuronal injury following complete cerebral ischemia. Acta Neuropathol 55:205–220

    Article  PubMed  CAS  Google Scholar 

  11. Jenkins LW, Becker DP (1982) A quantitative analysis of glial swelling and ischemic neuronal injury following complete cerebral ischemia. In: The proceedings of the 5th International Symposium on Brain Edema, Groningen, The Netherlands, in press

    Google Scholar 

  12. Jennings RB, Ganóte CE, Reimer KA (1975) Ischemic tissue injury. Am J Pathol 81:179–198

    PubMed  CAS  Google Scholar 

  13. Kalimo H, Garcia JH, Kamijyo Y, Tanaka J, Trump BF (1977) The ultrastructure of “brain death”. II. Electron microscopy of feline cortex after complete ischemia. Virchows Archiv Cell Pathol 25:207–220

    CAS  Google Scholar 

  14. Kalimo H, Paljärvi L, Vapalahti M (1979) The early ultrastructural alterations in the rabbit cerebral and cerebellar cortex after compression ischaemia. Neuropathol Appl Neurobiol 5:211–223

    Article  PubMed  CAS  Google Scholar 

  15. Kalimo H, Agardh C-D, Olsson Y, Siesjö BK (1980) Hypoglycemic brain injury. II. Electron microscopic findings in rat cerebral cortical neurons during profound insulin-induced hypoglycemia and in the recovery period following glucose administration. Acta Neuropathol 50:43–52

    Article  PubMed  CAS  Google Scholar 

  16. Kalimo H, Rehncrona S, Söderfeldt B, Olsson Y, Siesjö BK (1981) Brain lactic acidosis and ischemic cell damage: 2. Histopathology. J Cereb Blood Flow Metabol 1:313–327

    Article  CAS  Google Scholar 

  17. Kalimo H, Paljärvi L, Olsson Y (1982) Morphological and biochemical features of brain hypoxia-ischemia. In: Wauquier A. Ed. Protection of tissues against hypoxia. Elsevier, in press

    Google Scholar 

  18. Kimelberg HK, Bourke RS, Stieg PE, Barron KD, Hirata H, Peiton EW, Nelson LR (1982) Swelling of astroglia after injury to the central nervous system: Mechanisms and consequences: In: Grossman RG, Gildenberg PL. Eds. Head injury: Basic and clinical aspects. Raven, New York, pp 31–44

    Google Scholar 

  19. Kirino T (1982) Delayed neuronal death in the gerbil hippocampus following ischemia. Brain Res 239:57–69

    Article  PubMed  CAS  Google Scholar 

  20. Marcoux FW, Morawetz RB, Croweli RM, DeGirolami U, Halsey 3H (1982) Differential regional vulnerability in experimental focal cerebral ischemia. J Cereb Blood Flow Metabol 2:263

    Google Scholar 

  21. Myers RE (1977) Lactic acid accumulation as a cause of brain edema and cerebral necrosis resulting from oxygen deprivation. In: Korobkin R, Guilleminault G. Eds. Advances in Perinatal Neurology. Spectrum, pp 85–114

    Google Scholar 

  22. Pelligrino D, Alquist LO, Siesjö BK (1981) Effects of insulin-induced hypoglycemia on intracellular pH and impedance in the cerebral cortex of the rat. Brain Res 221:129–147

    Article  PubMed  CAS  Google Scholar 

  23. Petito CK, Babiak T (1982) Early proliferative changes in astroctyes in postischemic noninfarcted rat brain. Ann Neurol 11:510–518

    Article  PubMed  CAS  Google Scholar 

  24. Plum F (1982) What causes infarction in ischemic brain? Wartenberg lecture 1982, and personal communication

    Google Scholar 

  25. Pulsinelli WA, Brierley JB (1979) A new model of bilateral hemispheric ischemia in the unanesthetized rat. Stroke 10:267–272

    Article  PubMed  CAS  Google Scholar 

  26. Pulsinelli WA, Brierley JB, Plum F (1982) Temporal profile of neuronal damage in a model of transient forebrain ischemia. Ann Neurol 11:491–498

    Article  PubMed  CAS  Google Scholar 

  27. Pulsinelli WA, Levy DE, Sigsbee B, Scherer P, Plum F (1982) Hyperglycemia with or without established diabetes mellitus worsens stroke outcome. Am J Med, in press

    Google Scholar 

  28. Rehncrona S, Rosen I, Siesjö BK (1980) Excessive cellular acidosis: An important mechanism of neuronal damage in the brain? Acta Physiol Scand 110:435–437

    Article  PubMed  CAS  Google Scholar 

  29. Rehncrona S, Rosen I, Siesjö BK (1981) Brain lactic acidosis and ischemic cell damage: 1. Biochemistry and neurophysiology. J Cereb Blood Flow Metabol 1:297–311

    Article  CAS  Google Scholar 

  30. Siemkowicz E, Hansen AJ (1978) Clinical restitution following cerebral ischemia in hypo-, normo- and hyperglycemic rats. Acta Neurol Scand 58:1–8

    Article  PubMed  CAS  Google Scholar 

  31. Siemkowicz E, Hansen AJ, Gjedde A (1982) Hyperglycemic ischemia of rat brain: the effect of post-ischemic insulin on metabolic rate. Brain Res 243:386–390

    Article  PubMed  CAS  Google Scholar 

  32. Siesjö BK (1981) Cell damage in the brain: A speculative synthesis. J Cereb Blood Flow Metabol 1:155–185

    Article  Google Scholar 

  33. Söderfeldt B, Kalimo H, Olsson Y, Siesjö BK (1981) Pathogenesis of brain lesions caused by experimental epilepsy. Light-and electron-microscopic changes in the rat cerebral cortex following bicuculline-induced status epilepticus. Acta Neuropathol 54:219–231

    Article  PubMed  Google Scholar 

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© 1983 Springer-Verlag Berlin Heidelberg

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Kalimo, H., Paljärvi, L., Olsson, Y., Siesjö, B.K. (1983). Structural Aspects of Energy Failure States in the Brain. In: Wiedemann, K., Hoyer, S. (eds) Brain Protection. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-69175-1_1

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  • DOI: https://doi.org/10.1007/978-3-642-69175-1_1

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-642-69177-5

  • Online ISBN: 978-3-642-69175-1

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