Summary
Cerebral oxygenation was investigated during experimentally-induced status epilepticus to determine whether O2 supply is always sufficient to meet demand. Early in a series of seizures, cerebral oxygenation increased phasically in association with paroxysmal electrocortical activity. During later seizures, cerebral oxygenation decreased phasically, accompanied by attenuation of increases in cerebral blood flow, cerebral blood volume, and arterial blood pressure. The seizure-associated cerebral hypoxia occurred in many experiments without any changes in arterial PO2. Ventilation of the animal with 100% O2 restored the phasic increases in cerebral oxygenation, probably by restoring increases in cerebral blood flow. Systemic complications of status epilepticus (e.g., pulmonary edema) also can profoundly decrease cerebral oxygenation. An important remaining question is whether the cerebral hypoxia accompanying later seizures contributes to the neuronal damage following prolonged status epilepticus.
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© 1988 Plenum Press, New York
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Kreisman, N.R. (1988). Cerebral Hypoxia during Repetitive Seizures. In: Somjen, G. (eds) Mechanisms of Cerebral Hypoxia and Stroke. Advances in Behavioral Biology, vol 35. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5562-5_16
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DOI: https://doi.org/10.1007/978-1-4684-5562-5_16
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