Experimental cerebral oligemia and ischemia produced by intracranial hypertension. Part 3: Brain energy metabolism.
The authors studied the effect on cortical metabolites of intracranial hypertension produced by the infusion of mock cerebrospinal fluid into the cisterna magna in rabbits subjected to 15 minutes of cerebral oligemia (20 torr) or 15 minutes of complete ischemia. In both groups high-energy metabolites were exhausted within the first 5 minutes of the 15-minute insult. Significant recovery of the high-energy intermediates occurred within 15 minutes of reperfusion, well before return of electroencephalogram (EEG) activity. Continued reperfusion, during which electrical activity and function were returning, brought only moderate improvement in energy metabolites. In contrast, severe lactic acidosis persisted at least 15 minutes after insult, but was reduced by the time EEG activity returned. At no time were there striking differences in metabolites between the oligemic and ischemic groups. These results indicate that recovery in general, and the significantly earlier recovery of oligemic as compared to ischemic animals, cannot be explained on the basis of energy supply. Whether the persistence of lactic acidosis is an important factor limiting return of function requires further study.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001921:Brain / Q000098:blood supply*; D004569:Electroencephalography; D004734:Energy Metabolism; D005971:Glutamates / Q000378:metabolism; D007427:Intracranial Pressure; D007511:Ischemia / Q000378:metabolism*; D007773:Lactates / Q000378:metabolism; D010725:Phosphocreatine / Q000378:metabolism; D011817:Rabbits; D013997:Time Factors
D005971:Glutamates; D007773:Lactates; D010725:Phosphocreatine; D000255:Adenosine Triphosphate