Oxidative metabolic responses with recurrent seizures in rat cerebral cortex: role of systemic factors.
Simultaneous focal measurements of cerebral oxygen tension and cytochrome a,a3 redox levels were made in rat cortex in order to obtain a direct and continuous assessment of oxidative metabolic changes during serial seizures. Initial seizures evoked by pentylenetetrazol were accompanied by transient increases in tissue pO2 and cytochrome a,a3 oxidation, confirming that oxygen provision is adequate to meet metabolic demand. After some point, subsequent seizures were accompanied by failure of pO2 to increase and failure of cytochrome a,a3 to oxidize, or by decreases in tissue pO2 and shifts in the redox level of cytochrome a,a3 toward reduction, signalling cortical oxygen insufficiency. Whereas early seizures were accompanied by increments in both cerebral blood volume and arterial blood pressure, one or both of these variables failed to increment during later seizures. This was particularly evident following the onset of spontaneously recurring seizures with short intervals between bursts of ECoG activity. These investigations emphasize the importance of systemic factors in determining the cerebral metabolic response to seizures and support the suggestion that neuronal damage in status epilepticus may be the result of derangements of oxidative metabolism.
D000818:Animals; D001794:Blood Pressure; D001810:Blood Volume; D002540:Cerebral Cortex / Q000378:metabolism*; D003576:Electron Transport Complex IV / Q000378:metabolism; D010084:Oxidation-Reduction; D010101:Oxygen Consumption; D010313:Partial Pressure; D010433:Pentylenetetrazole; D051381:Rats; D012640:Seizures / Q000139:chemically induced / Q000378:metabolism*
D003576:Electron Transport Complex IV; D010433:Pentylenetetrazole