Hyperthermic preconditioning prevents blood-brain barrier disruption produced by hypoxia-ischemia in newborn rat

Effect of hyperthermic preconditioning on disruption of blood-brain barrier induced by hypoxic-ischemic insult was examined. Seven-day-old Wistar rats were separated into (1) pre-heated (15 min of hyperthermia at 41.5-42.0 degrees C) or (2) non-heated group (33 degrees C). Twenty-four hours after conditioning, all rats were subjected to 2 h hypoxia-ischemia (8% oxygen/92% nitrogen, at 33 degrees C), then 24 h later all brains were examined for immunohistological staining of endogenous macromolecule, IgG extravasation and staining of microtubule-associated protein 2 (MAP2) with MAP2 loss being an early marker of neuronal damage. Significant reduction in the area of IgG staining and loss of MAP2 staining was observed in the pre-heated group as compared to that in non-heated group. There was a close relationship between IgG staining and MAP2 staining loss, with the former area always found in the latter, suggesting that extravasation associates neuronal injury. Serum cortisol concentration in pre-heated group was significantly higher than that in non-heated group 24 h after hyperthermic treatment (14.8+/-0.6 vs. 12.5+/-0.3 ng/ml, p<0.01). These data indicate that hyperthermic preconditioning prevents disruption of blood-brain barrier, resulting in amelioration of hypoxic-ischemic neuronal damage in newborn rat.