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Morphological Responses of Cerebral Tissues to Temporary Ischemia

Published online by Cambridge University Press:  18 September 2015

Ronald F. Dodson ,
Yukio Tagashira ,
Yasuo Kawamura  and
Lena Wai-Fong Chu
Ronald F. Dodson*
Affiliation:
Departments of Neurology and Pathology, Baylor College of Medicine and the Baylor-Methodist Center for Cerebrovascular Research, Houston, Texas 77025
Yukio Tagashira
Affiliation:
Departments of Neurology and Pathology, Baylor College of Medicine and the Baylor-Methodist Center for Cerebrovascular Research, Houston, Texas 77025
Yasuo Kawamura
Affiliation:
Departments of Neurology and Pathology, Baylor College of Medicine and the Baylor-Methodist Center for Cerebrovascular Research, Houston, Texas 77025
Lena Wai-Fong Chu
Affiliation:
Departments of Neurology and Pathology, Baylor College of Medicine and the Baylor-Methodist Center for Cerebrovascular Research, Houston, Texas 77025
*
Department of Neurology, Baylor College of Medicine, 1200 Moursund Avenue, Houston, Texas 77025
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Summary:

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The ultrastructural responses of cerebral tissue following temporary periods (½, 1, 2, 3, or 4 hour) of right, middle cerebral artery, (MCA) occlusion were studied acutely after a 3 day or 7 day interval following the removal of the MCA clip. Cortical and basal ganglia tissues for each ischemic duration were compared at 3 post-occlusive periods (acute, 3 days, 7 days).

With the short periods of ischemic insult (½, 1, 2, 3, and 4 hour), the temporal and insular cortex contained no greater changes in the 7 day group than in the 3 day group.

The basal ganglia were more susceptible to MCA occlusion as indicated by more marked cytological changes and/or necrosis in all intervals of ischemia.

Type
Research Article
Information
Canadian Journal of Neurological Sciences , Volume 2 , Issue 3 , August 1975 , pp. 173 - 177
Copyright
Copyright © Canadian Neurological Sciences Federation 1975

References

REFERENCES

Dodson, R.F., Kawamura, Y., Aoyagi, M.Hartmann, A. and Cheung, L. (1973). A comparative evaluation of the ultrastructural changes following induced cerebral infarction in squirrel monkey and baboon. Cytobios, 8: 175–182.Google ScholarPubMed
Drewes, L.R., Gilboe, D.D. and Betz, A.L. (1973). Metabolic alterations in brain during anoxic-anoxia and subsequent recovery. Arch. Neurol., 29: 385–390.CrossRefGoogle ScholarPubMed
Garcia, J.H., Cox, J.V. and Hudgins, W.R. (1971). Ultrastructure of the microvasculature in experimental cerebral infarction. Acta Neuropath., 18: 273–285.CrossRefGoogle ScholarPubMed
Garcia, J.H. and Kamijyo, Y. (1974). Cerebral Infarction: Evolution of Histopathological changes after occlusion of a middle cerebral artery in primates. J. Neuropath. Exptl. Neurol., 33: 408–421.CrossRefGoogle ScholarPubMed
Ghidoni, J.J., Campbell, M.M., Adams, J.G., Thomas, H. and Ramos, E.E. (1968). A new multicolor staining procedure for one micron sections of epoxy embedment. Electron Microscopy Soc. Amer. Proc, 240–241.CrossRefGoogle Scholar
Hossmann, K-A (1972). Recovery of the cat brain after transient ischemia. In Meyer, J.S., Reivich, M.Lechner, H. and Erichhorn, O. (eds): Research on the Cerebral Circulation, C. C. Thomas, Illinois, p. 103–111.Google Scholar
Hossmann, K-A and Kleihues, P. (1973). The recoverability of ischemic brain damage. Arch. Neurol., 29: 375–384.CrossRefGoogle Scholar
Hossmann, K-A and Zimmermann, V. (1974). Resuscitation of the monkey brain after 1 hr. complete ischemia 1. Physiological and morphological observations. Brain Res., 81: 59–74.Google Scholar
Hudgins, W.R. and Garcia, J.H. (1970). Transorbital approach to the middle cerebral artery of the squirrel monkey: a technique for experimental cerebral infarction applicable to ultrastructural studies. Stroke, 1: 107–111.CrossRefGoogle Scholar
Klatzo, I. (1967). Neuropathological aspects of brain edema. J. Neuropath. Exptl. Neurol., 26: 1–14.CrossRefGoogle ScholarPubMed
Lanner, G.Lechner, H. and Ott, E. (1972). The isoelectric EEG-dependence on the duration of ischemia: An experimental contribution. In Meyer, J.S., Reivich, M.Lechner, H. and Echhorn, O. (eds.): Research on Cerebral Circulation, C. C. Thomas, Illinois, p. 112–121.Google Scholar
Miller, J.R. and Myers, R.E. (1972). Neuropathology of systemic circulatory arrest in adult squirrel monkeys. Neurology 22: 888–904.CrossRefGoogle Scholar
Ng, L.K.Y. and Nimmannitya, J. (1970). Massive cerebral infarction with brain swelling: clinicopathological study. Stroke 1: 158–163.CrossRefGoogle ScholarPubMed
Plum, F. (1964). Brain swelling and edema in cerebral vascular disease. Proc. Assoc. Res. New. Ment. Dis., 41: 318–348.Google Scholar
Plum, F. (1973). The clinical problem: How much anoxia-ischemia damages the brain? Arch. Neurol., 29: 359–360.Google Scholar
Shaw, C.M., Alvord, E.C. Jr. and Berry, R.G. (1959). Swelling of brain following ischemic infarction with arterial occlusion. Arch. Neurol. 1: 161–177.Google Scholar
Spurr, A.R. (1969). A low-viscosity epoxy resin embedding medium for electron microscopy. J. Ultrastruct. Res., 26: 31–43.CrossRefGoogle ScholarPubMed
Sundt, T.M., Grant, W.C. and Garcia, J.H. (1969). Restoration of middle cerebral artery flow in experimental infarction. J. Neurosurg., 31: 311–322.CrossRefGoogle ScholarPubMed