A Quantitative Analysis of Glial Swelling and Ischemic Neuronal Injury Following Complete Cerebral Ischemia
Prior studies have demonstrated that a transformation in neuronal structural responses occurs during the reperfusion period following complete cerebral ischemia (CCI)10,11,12,14. ThE homo-geneous pattern of neuronal injury seen with permanent CCI is modified into a heterogeneous pattern of “selectively vulnerable” neuronal responses with recirculation10,11. The events which cause this transformation remain poorly understood. In addition to such neuronal responses, the glial population of the brain also displays characteristic structural changes, Oligodendrocytes are resistent to significant structural change compared to neurons, but astrocy-tes show an early enlargement of perineuronal and perivascular pro-cesses10,11,12,14,15,8. The anatomical relationships which exist between the neuronal, astrocytic and vascular compartments make any enlargement in the astrocytic compartment a factor of potential importance2,3,17,16. Yet, few morphological studies have attempted to quantify astrocytic changes or relate such alterations to neuronal responses following CCI. Perivascular glial swelling has been implicated as one of the causes of reperfusion defects following CCI4,13,1,9. but subsequent experimental evidence has not confirmed this view5,7,6. Recent studies have proposed that even in the absence of any direct vascular effect, astrocytic swelling may increase the critical diffusion pathway for substrate, metabolite and gas exchange between the vascular and neuronal compartments2,3,16. The purpose of the present investigation was to quantify the distribution of the above neuronal and astrocytic responses after various durations of CCI and postischemic recirculation. Additionally, plasma or blood substitute reperfusion following CCI was evaluated to determine the effect of electrolyte, fluid and oxygen restitution upon the completely ischemic brain.
KeywordsNeuronal Response Tyrodes Solution Blood Substitute Ischemic Neuronal Injury Gallamine Triethiodide
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- 3.Bourke RS, Kimelberg HK, Nelson LR, Barron KD, Auen EL, Popp AJ, Waldman JB: Biology of glial swelling in experimental brain edema. In: Brain edema; Cervos-Navarro J, Ferszt R (Eds), Raven Press, New York. Adv Neurol 28 99–109 (1980).Google Scholar
- 4.Chiang J, Kowada MG, Ames III A, Wright RL, Majno G: Cerebral Ischemia III Vascular changes. Am J Pathol 52 455–476 (1968).Google Scholar
- 7.Garcia JH, Lossinsky AS, Nishimoto K, Klatzo I, Lightfoot jr W: Cerebral microsvasculature in ischemia. Adv Neurol 20 141–149 (1979).Google Scholar
- 8.Garcia JH, Conger KA, Morawetz R, Halsey Jr JH: Postischemic Brain Edema. Quantitation and evolution. In: Brain edema, Cervos-Navarro J, Ferszt R (Eds), Raven Press, New York. Adv Neurol 28 147–169 (1980).Google Scholar
- 12.Kalimo H, Garcia JH, Kamijyo, Y Tanaka J, Trump BF: The ultra-structure of “Brain death”. II. Electron microscopy of feline cortex after complete ischemia. Virchows Arch B (Cell Pathol) 25 207–220 (1977).Google Scholar
- 14.Shay J: Morphometry of an ischemic lesion of cat spinal cord. Am J Pathol 72 397–402 (1973).Google Scholar
- 15.Shay J, Gontas NK: Electron microscopy of cat spinal cord subject to circulatory arrest and deep local hypothermia (15 C). Am J Pathol 72 369–396 (1972).Google Scholar