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| [There is a suggestion that the high potassium concentration] in the ischemic focus initiates diffusion of K+ into the adjacent normally perfused cortex and triggers SD waves propagating from the rim of the focus to the surrounding intact tissue during the early stages of focal ischemia (Nedergaard and Astrup, 1986). Local reduction of tissue glucose content, caused by the increased demands and reduced supply of glucose in the area, might further reduce the threshold for elicitation of SD. In subsequent minutes and hours, further SD waves can be generated from the boundary of the focus provided that the chemical gradient is steep enough to support sufficiently intensive diffusion of active substances into the intact cortex (Hossmann, 1996). A SD wave initiated from a single point at the periphery of the focus spreads away from it but may turn around and enter the penumbra zone in a different area of the focus. Generation of SD is limited to an approximately 2-h period after ischemia, followed by a shorter interval of increased SD susceptibility which disappear 3-4 h after the onset of focal ischemia (Koroleva et al., 1998). Such SD waves significantly longer than those occurring in intact cortex and can be potentially harmful because they are accompanied by additional release of glutamate and influx of calcium into the neurons. In normal brain tissue, repeated SD waves do not induce any morphological or metabolic damage. However, it is believed that when SD repeatedly collapses ionic gradients, activation of NMDA receptors and gap junctions propagates SD and triggers a massive Ca2+ influx, which in energy-compromised neurons is enough to initiate a cell death cascade (Somjen et al., 1990). The tissue fully recovers when SD induced by elevating K+ in rat hippocampal slices, but in slices that are metabolically compromised by oxygen/glucose deprivation, cellular damage develops only where SD has propagated. After propagating SD in oxygen/glucose-deprived tissues, the evoked CA1 field potential is permanently lost, the cell bodies of involved neurons swell and their dendritic regions increase in opacity (Obeidat and Andrew, 1998).
SD can serve as a marker of normal function of SD-prone cerebral tissue. It disappears in cortical regions in which neuronal density was reduced by ischemia and can be used for appreciation of delayed recovery or deterioration in the penumbra zone after focal ischemia. Several studies showed that in focal brain ischemia SD increases the ischemic volume. The pathogenic importance of peri-infarct depolarizations for the progression of ischemic injury is supported by the close linear correlation between number of SD and the duration of elevated potassium with infarct volume and reduction of infarct size and neuronal loss in penumbra area by application of NMDA and non- NMDA receptor antagonist and by hypothermia (Mies et al., 1993; Mies et al., 1994). Hossmann KA (1996) Periinfarct depolarizations. Cerebrovasc Brain Metab Rev 8(3):195-208. Koroleva VI, Vinogradova LV, Korolev OS (1998) The persistent negative potential provoked in different structures of the rat brain by a single wave of spreading cortical depression. Zh Vyssh Nerv Deiat Im I P Pavlova. 48(4):654-63. Mies G, Iijima T, Hossmann KA (1993) Correlation between peri-infarct DC shifts and ischaemic neuronal damage in rat. Neuroreport 4(6):709-11. Mies G, Kohno K, Hossmann KA (1994) Prevention of periinfarct direct current shifts with glutamate antagonist NBQX following occlusion of the middle cerebral artery in the rat. J Cereb Blood Flow Metab. 14(5):802-7. Nedergaard M, Vorstrup S, Astrup J (1986) Cell density in the border zone around old small human brain infarcts. Stroke 17(6):1129-37. Obeidat AS, Andrew RD (1998) Spreading depression determines acute cellular damage in the hippocampal slice during oxygen/glucose deprivation. Eur J Neurosci 10(11):3451-61. Somjen GG, Aitken PG, Balestrino M, Herreras O, Kawasaki K (1990) Spreading depression-like depolarization and selective vulnerability of neurons. A brief review. Stroke 21(11 Suppl):III179- 83. |
There is a suggestion that the high potassium concentration in the ischemic focus initiates diffusion of K+ into the adjacent normally perfused cortex and triggers SD waves propagating from the rim of the focus to the surrounding intact tissue during the early stages of focal ischemia [301,395]. Local reduction of tissue glucose content, caused by the increased demands and reduced supply of glucose in the area, might further reduce the threshold for elicitation of SD. In subsequent minutes and hours, further SD waves can be generated from the boundary of the focus provided that the chemical gradient is steep enough to support sufficiently intensive diffusion of active substances into the intact cortex [179]. A SD wave initiated from a single point at the periphery of the focus spreads away from it but may turn around and enter the penumbra zone in a different area of the focus. Generation of SD is limited to an approximately 2-h period after ischemia, followed by a shorter interval of increased SD susceptibility which disappear 3-4 h after the onset of focal ischemia [218]. Such SD waves significantly longer than those occurring in intact cortex and can be potentially harmful because they are accompanied by additional
[page 44] release of glutamate and influx of calcium into the neurons. In normal brain tissue, repeated SD waves do not induce any morphological [404] or metabolic [148,170] damage. However, it is believed that when SD repeatedly collapses ionic gradients, activation of NMDA receptors and gap junctions propagates SD and triggers a massive Ca2+ influx, which in energy-compromised neurons is enough to initiate a cell death cascade [180,404]. The tissue fully recovers when SD induced by elevating K+ in rat hippocampal slices, but in slices that are metabolically compromised by oxygen/glucose deprivation, cellular damage develops only where SD has propagated. After propagating SD in oxygen/glucose-deprived tissues, the evoked CA1 field potential is permanently lost, the cell bodies of involved neurons swell and their dendritic regions increase in opacity [311]. SD can serve as a marker of normal function of SD-prone cerebral tissue. It disappears in cortical regions in which neuronal density was reduced by ischemia and can be used for appreciation of delayed recovery or deterioration in the penumbra zone after focal ischemia [218,219]. Several studies showed that in focal brain ischemia SD increases the ischemic volume. The pathogenic importance of peri-infarct depolarizations for the progression of ischemic injury is supported by the close linear correlation between number of SD and the duration of elevated potassium with infarct volume and reduction of infarct size and neuronal loss in penumbra area by application of NMDA and non-NMDA receptor antagonist and by hypothermia [281,282,359]. [148] N.A. Gorelova, J. Krivanek, J. Bures, Functional and metabolic correlates of long series of cortical spreading depression waves in rats, Brain Res. 404 (1987) 379-381. [170] A.J. Hansen, M. Nedergaard, Brain ion homeostasis in cerebral ischemia, Neurochem. Pathol. 9 (1988) 195-209. [179] K.A. Hossmann, Periinfarct depolarizations, Cerebrovasc. Brain Metab. Rev. 8 (1996) 195-208. [180] K.A. Hossmann, Mechanisms of ischemic injury: is glutamate involved?, in: J. Krieglstein, H. Oberpichler-Schwenk (Eds.), Pharmacology of Cerebral Ischemia, Medpharm Scientific, Stuttgart, 1994, pp. 239-251. [218] VI. Koroleva, J. Bures, TPe use of spreading depression waves for acute and long-term monitoring of the penumbra zone of focal ischemic damage in rats, Proc. Natl. Acad. Sci. USA 93 (1996) 3710-3714. [219] VI. Koroleva, O.S. Korolev, E. Loseva, J. Bures, TPe effect of MK-801 and of brain-derived polypeptides on the development of ischemic lesion induced by photothrombotic occlusion of the distal middle cerebral artery in rats, Brain Res. 786 (1998) 104-114. [281] G. Mies, K. Kohno, K.A. Hossmann, MK-801, a glutamate antagonist, lowers flow threshold for inhibition of protein synthesis after middle cerebral artery occlusion of rat, Neurosci. Lett. 155 (1993) 65-68. [282] G. Mies, K. Kohno, K.A. Hossmann, Prevention of periinfarct direct current shifts with glutamate antagonist NBQX following occlusion of the middle cerebral artery in the rat, J. Cereb. Blood Flow Metab. 14 (1994) 802-807. [301] M. Nedergaard, J. Astrup, Infarct rim: effect of hyperglycemia on direct current potential and [14C]2-deoxyglucose phosphorylation, J. Cereb. Blood Flow Metab. 6 (1986) 607-615. [311] A.S. Obeidat, R.D. Andrew, Spreading depression determines acute cellular damage in the hippocampal slice during oxygen/glucose deprivation, Eur. J. Neurosci. 10 (1998) 3451-3461. [359] K. Revett, E. Ruppin, S. Goodall, J.A. Reggia, Spreading depression in focal ischemia: a computational study, J. Cereb. Blood Flow Metab. 18 (1998) 998-1007. [395] B.K. Siesjo, F. Bengtsson, Calcium fluxes, calcium antagonists, and calcium-related pathology in brain ischemia, hypoglycemia, and spreading depression: a unifying hypothesis, J. Cereb. Blood Flow Metab. 9 (1989) 127-140. [404] G.G. Somjen, P.G. Aitken, M. Balestrino, O. Herreras, K. Kawasaki, Spreading depression-like depolarization and selective vulnerability of neurons. A brief review, Stroke 21 (11 S) (1990) III-179-183. |
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