TEMPORAL EVOLUTION OF NEUROPATHOLOGIC CHANGES IN AN IMMATURE RAT MODEL OF CEREBRAL HYPOXIA - A LIGHT-MICROSCOPIC STUDY

Citation
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
Citations number
34
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
00016322
Volume
90
Issue
4
Year of publication
1995
Pages
375 - 386
Database
ISI
SICI code
0001-6322(1995)90:4<375:TEONCI>2.0.ZU;2-O
Abstract
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.