T. Ikeda et al., Hyperthermic preconditioning prevents blood-brain barrier disruption produced by hypoxia-ischemia in newborn rat, DEV BRAIN R, 117(1), 1999, pp. 53-58
Effect of hyperthermic preconditioning on disruption of blood-brain barrier
induced by hypoxic-ischemic insult was examined. Seven-day-old Wister rats
were separated into (1) pre-heated (15 min of hyperthermia at 41.5-42.0 de
grees C) or (2) non-heated group (33 degrees C). Twenty-four hours after co
nditioning, 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 im
munohistological staining of endogenous macromolecule, IgG extravasation an
d staining of microtubule-associated protein 2 (MAP2) with MAP2 loss being
an early marker of neuronal damage. Significant reduction in the area of Ig
G staining and loss of MAP2 staining was observed in the pre-heated group a
s compared to that in non-heated group. There was a close relationship betw
een IgG staining and MAP2 staining loss, with the former area always found
in the latter, suggesting that extravasation associates neuronal injury. Se
rum cortisol concentration in pre-heated group was significantly higher tha
n 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 pr
econditioning prevents disruption of blood-brain barrier, resulting in amel
ioration of hypoxic-ischemic neuronal damage in newborn rat. (C) 1999 Elsev
ier Science B.V. All rights reserved.