Abstract
According to statistical analyses of stroke cases in intensive care units, about 70% of cerebrovascular accidents are the results of vascular occlusive diseases of various origins (mainly embolic or thrombotic) (Hachinski and Norris, 1981). The majority of brain infarcts occur in the territory of the middle cerebral artery (MCA), the pathological consequences being found in the insular cortex and basal ganglia. Whereas it is commonly accepted that the primary ischemic focus is irreversibly damaged, increasing interest is being devoted to the surrounding tissue, which is still viable. In fact, maintaining the collateral circulation should be of benefit to the infarct area and restrict the extension of ischemia into adjoining tissue.
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References
Blöink, M., Hossmann, V., and Hossmann, K.A., 1980, Treatment of experimental infarcts following middle cerebral artery occlusion in cats, in; “Circulation Cérébrale”, Proc. Congrès International de Circulation Cérébrale, 1979, A. Bès, C. Géraud, eds., Toulouse.
Bremer, A., West, C.R., and Yamada, K., 1979, Alterations in cortical oxygen tension during the development of ischemic cerebral edema in primates, Neurosurgery, 4: 233.
Cahn, R., Poncin, J.F., and Pawelec, C., 1980, Brain cortical Po2, EEG activity, cerebral (A-V) lactate and ultrastructural changes in temporary middle cerebral artery occlusion in chloralose anaesthetized mongrel dogs, in: “Pathophysiology and Pharmacotherapy of Cerebrovascular Disorders”, A. Betz, J. Grote, D. Heuser, R. Wüllenweber, eds., Witzstrock, Baden-Baden, p. 187.
Crockard, H.A., Symon, L., Branston, N.M., and Juhasz, J., 1976, Changes in regional cortical tissue oxygen tension and cerebral blood flow during temporary middle cerebral artery occlusion in baboons, J. Neurol. Sci., 27: 29.
Crowell, R.M., and Olsson, Y., 1972, Impaired microvascular filling after focal cerebral ischemia in the monkey. Modification by treatment, Neurology, 22: 500.
Hachinski, V., and Norris, J.W., 1981, Intensive care of stroke, in: “Drugs and Methods in CVD”, Pergamon Press, Paris, p. 375.
Harris, R.J., Symon, L., Branston, N.M., and Bayhan, M., 1981, Changes in extracellular calcium activity in cerebral ischemia, J. Cereb. Blood Flow Metab., 1: 203.
Ingvar, M.C., Feustel, P.J., Brenneman, L., and Severinghaus, J.W., 1980, Local cerebral blood flow and oxygen availability measured with the same 25 micron electrodes in cat cortex before and during middle cerebral artery ligation at altered Pco2 levels, in: “Cerebral Blood Flow and Metabolism”, F. Gotoh, H. Nagai, Y. Tazaki, eds., Munksgaard, Copenhagen, pp. 5–7.
Kamijyo, Y., Garcia, J.H., and Cooper, J., 1977, Temporary regional cerebral ischemia in the cat, J. Neuropathol. Exp. Neurol., 36: 337.
Little, J.R., Cook, A., Cook, S.A., and McIntyre, W.J., 1981, Micro-circulatory obstruction in focal cerebral ischemia: albumin and erythrocyte transit, Stroke, 12: 218.
Little, J.R., and O’Shaughnessy, D., 1979, Treatment of acute focal ischemia with continuous CSF drainage and mannitol, Stroke, 10: 446.
Peerless, S.J., Ishikawa, R., Hunter, I.G., and Peerless, M.J., 1981, Protective effect of Fluosol-DA in acute cerebral ischemia, Stroke, 12: 558.
Ravvin, L.J., Feindel, W., Yamamoto, Y.L., and Hodge, C.P., 1977, Epicerebral arterial occlusion in the dog, in: “Cerebral Function, Metabolism and Circulation”, D.H. Ingvar, N.A. Lassen, eds., Munksgaard, Copenhagen, p. 363.
Schuier, F.J., and Hossmann, K.A., 1980, Experimental brain infarcts in cats. II. Ischemic brain edema, Stroke, 11: 593.
Sundt, T.M., and Waltz, A.G., 1967, Hemodilution and anticoagulation. Effects on the microvasculature and microcirculation of the cerebral cortex after arterial occlusion, Neurology, 17: 230.
Tamura, A., and Teasdale, G., 1980, Effects of perivascular micro-application of Nifedipine on cat pial arteriolar and venular caliber, in: “Pathophysiology and Pharmacotherapy of Cerebrovascular Disorders”, E. Betz, J. Grote, D. Heuser, R. Wüllen-weber, eds., Witzstrock, Baden-Baden, p. 19.
Theodore, D., and Abraham, J., 1980, A sequentious study of capillaries in the infarcted area of primate brain, Ind. J. Med. Res., 71: 821–828.
Wiernsperger, N., and Gygax, P., 1981, Determination of tissular Po2 in brain microvascular research, Eur. Neurol, 20: 200.
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© 1984 Plenum Press, New York
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Wiernsperger, N. (1984). Focal Epicerebral Ischemia: Post-Ischemic Tissue Oxygenation with and without Recirculation. In: Lübbers, D.W., Acker, H., Leniger-Follert, E., Goldstrick, T.K. (eds) Oxygen Transport to Tissue-V. Advances in Experimental Medicine and Biology, vol 169. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-1188-1_19
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DOI: https://doi.org/10.1007/978-1-4684-1188-1_19
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