PREISCHEMIC HYPERGLYCEMIA LEADS TO DELAYED POSTISCHEMIC HYPERTHERMIA

Background and Purpose Temperature alterations are known to influence the outcome of transient ischemia, even when instituted in the postisc hemic period. Since preischemic hyperglycemia aggravates ischemic brai n damage, the question of whether hyperglycemic animals become hyperth ermic arose. To explore this possibility, we measured body temperature telemetrically in normoglycemic and hyperglycemic rats subjected to 1 0 minutes of forebrain ischemia at a body (and brain) temperature of 3 7 degrees C. Methods Isoflurane-anesthetized animals were subjected to 10 minutes of forebrain ischemia under normoglycemic or hyperglycemic conditions. Temperature changes after ischemia were measured by means of a telemetric temperature coil. Results In normoglycemic animals, t emperature decreased to 35.6+/-1.1 degrees C (mean+/-SD) during the fi rst 4 hours of recovery, after which it gradually increased to normal values (38 degrees C). Hyperglycemic animals behaved differently in th at they remained normothermic for approximately 10 hours during recove ry and later became hyperthermic, with core temperatures rising above 39 degrees C. The rise in temperature was not due to the osmotic load of the glucose administered because infusion of mannitol, which gave a comparable increase in plasma osmolality, failed to cause delayed pos tischemic hyperthermia. Excessive hypercapnia during ischemia in normo glycemic animals, which produces cerebral acidosis of a magnitude simi lar to that of hyperglycemia and is known to aggravate ischemic lesion s, likewise failed to induce hyperthermia. When post ischemic seizures ensued in hyperglycemic subjects, temperature was 39.8+/-0.6 degrees C. Animals with seizures invariably died. To evaluate the influence of postischemic hyperthermia on the outcome, an additional series of exp eriments was performed in which delayed hyperthermia was avoided by ge ntle cooling (n=6) or by acetaminophen administration (n=5). Although these procedures prevented delayed hyperthermia, they neither blocked seizure induction nor affected the fatal outcome. Postischemic seizure s developed when the core temperatures of animals were 37.9+/-0.1 degr ees C and 37.8+/-0.2 degrees C in the cooled and acetaminophen-treated groups, respectively. Conclusions The results suggest that both delay ed hyperthermia and delayed seizures in hyperglycemic animals are caus ed by the aggravated damage incurred by these animals during or immedi ately after the ischemic insult.