J. Towfighi et al., TEMPORAL EVOLUTION OF NEUROPATHOLOGIC CHANGES IN AN IMMATURE RAT MODEL OF CEREBRAL HYPOXIA - A LIGHT-MICROSCOPIC STUDY, Acta Neuropathologica, 90(4), 1995, pp. 375-386
The sequential evolution of neuropathologic changes was studied in an
immature model of cerebral hypoxia-ischemia. Accordingly, 7-day postna
tal rats were subjected to unilateral common carotid artery ligation c
ombined with 2 h of hypoxia (breathing in 8% oxygen) and their brains
were examined by light microscopy at recovery intervals ranging from 0
to 3 weeks. Immediately following hypoxia, a large area with a pale s
taining border was noted occupying most of the cerebral hemisphere ips
ilateral (IL) to the occluded common carotid artery; in approximately
half of the brains the dorsomedial cortex of the contralateral (CL) he
misphere was also involved. Most neurons in the pale area had nuclei c
ontaining a coarse granular condensation of chromatin. Within a few ho
urs, the majority of neurons in the IL hemisphere had developed pyknot
ic nuclei and clear or eosinophilic perikarya. After 24 h these change
s had evolved in the majority of brains into coagulation necrosis (inf
arction) in the IL hemisphere and foci of selective neuronal necrosis
in the CL cortex. Within a few days infarcts became partially cavitate
d, and by 3 weeks a smooth-walled cystic infarct had developed. Activa
ted microglia/macrophages and reactive astrocytes were first seen at 4
and 24 h, respectively. No parenchymal neutrophilic infiltrate was se
en at any time point.