FUNCTIONAL, METABOLIC, AND CIRCULATORY CHANGES ASSOCIATED WITH SEIZURE ACTIVITY IN THE POSTISCHEMIC BRAIN

The present study was undertaken to explore how transient ischemia in rats alters cerebral metabolic capacity and how postischemic metabolis m and blood flow are coupled during intense activation. After 6 h of r ecovery following transient forebrain ischemia 15 min in duration, bic uculline seizures were induced, and brains were frozen in situ after 0 .5 or 5 min of seizure discharge. At these times, levels of labile tis sue metabolites were measured, whereas the cerebral metabolic rate for oxygen (CMRO2) and cerebral blood flow (CBF) were measured after 5 mi n of seizure activity. After 6 h of recovery, and before seizures, ani mals had a 40-50% reduction in CMRO2 and CBF. However, because CMRO2 r ose three-fold and CBF fivefold during seizures, CMRO2 and CBF during seizures were similar in control and postischemic rats. Changes in lab ile metabolites due to the preceding ischemia encompassed an increased phosphocreatine/creatine ratio, as well as raised glucose and glycoge n concentrations. Seizures gave rise to minimal metabolic perturbation , essentially comprising reduced glucose and glycogen contents and rai sed lactate concentrations. It is concluded that although transient is chemia leads to metabolic depression and a fall in CBF, the metabolic capacity of the tissue is retained, and drug-induced seizures lead to a coupled rise in metabolic rate and blood flow.