Summary
Isolated canine brains were subjected to either 30 min of anoxic anoxia (perfusion with blood having a pO2 < 10 mm Hg) or ischemia (no perfusion). Brain oxidative metabolism, unidirectional and net glucose transport, adenine nucleotide, water and electrolyte content were studied during a 2 h period of re-perfusion.
Although anoxic and ischemic brain preparations both have lower than normal rates of metabolism following the insult, the anoxic preparation is the more severely depressed. Cerebral edema is observed in tissue taken from the cortex of both preparations; however, brains subjected to ischemia become less edematous during re-perfusion. ATP levels are approximately 55% of normal in both preparations; thus ATP content does not appear to be directly related to the ability to recover from edema.
The slower rate of metabolism in the anoxic preparations may be due to the presence of abnormally high amounts of lactate in the tissues. Although this pH effect could slow Na/K ATPase activity, the failure to recover rapidly may be a consequence of more severe glial cell damage in the anoxic brains.
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Gilboe, D.D., Drewes, L.R., Kintner, D. (1976). Edema Formation in the Isolated Canine Brain: Anoxia vs. Ischemia. In: Pappius, H.M., Feindel, W. (eds) Dynamics of Brain Edema. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-66524-0_36
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DOI: https://doi.org/10.1007/978-3-642-66524-0_36
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