A histological and flow cytometric study of dog brain endothelial cell injuries in delayed radiation necrosis

Journal Article · Mon Apr 01 00:00:00 EST 1991 · Journal of Neurosurgery; (USA)

DOI:https://doi.org/10.3171/jns.1991.74.4.0625· OSTI ID:5952132

Yamaguchi, N; Yamashima, T; Yamashita, J ^[1]

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1. Kanazawa Univ. School of Medicine (Japan)

The pathogenesis of delayed cerebral radiation necrosis was studied histologically and biochemically in 25 dogs with special attention to vascular endothelial cell injuries. The dogs were sacrificed 3 to 30 months after irradiation with a single dose of 15 Gy to the head. Brain specimens were appropriately fixed for light and electron microscopic studies, and capillary endothelial cells were isolated for flow cytometric study. The endothelial cells were stained with acridine orange, then the cell ratios in the reproductive phase (S + G2 + M) were investigated with flow cytometry. Thereafter, Feulgen hydrolysis and computer analysis of the hydrolysis curves were performed to examine the qualitative changes in deoxyribonucleic acid (DNA) of endothelial cells after irradiation. Under light microscopy, spongy degeneration with small cell infiltration was observed, especially in the frontal white matter, at 6 months after irradiation. At 9 months, necrotic foci appeared and developed until 15 months after irradiation. Blood vessels around the necrotic area showed luminal narrowing with endothelial hyperplasia and proliferation. At 30 months, no fresh necrotic lesions were observed. Under electron microscopy, endothelial cells of capillaries and small vessels around the necrotic area showed an increase of pinocytosis, and in the nuclei there was an increase of infoldings and euchromatin. The cell ratios in the reproductive phase were 14.5% to 23.3% (maximum at 9 months) in the irradiated group compared to 6.4% in the control group. The rate constant of apurinic acid production, a parameter correlating with DNA transcriptional activity, was minimum at 3 months and maximum at 9 months after irradiation. The data suggest that impairment of the microcirculation plays an important role in the pathogenesis of delayed radiation necrosis.

• OSTI ID: 5952132
• Journal Information: Journal of Neurosurgery; (USA), Vol. 74:4; ISSN 0022-3085
• Country of Publication: United States
• Language: English

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63 RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT.
ENDOTHELIUM
DELAYED RADIATION EFFECTS
NERVOUS SYSTEM DISEASES
PATHOGENESIS
CAPILLARIES
CELL CYCLE
CELL FLOW SYSTEMS
DNA
DOGS
NECROSIS
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ANIMAL TISSUES
ANIMALS
BIOLOGICAL EFFECTS
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BLOOD VESSELS
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DISEASES
INJURIES
MAMMALS
NUCLEIC ACIDS
ORGANIC COMPOUNDS
ORGANS
PATHOLOGICAL CHANGES
RADIATION EFFECTS
TISSUES
VERTEBRATES
560152* - Radiation Effects on Animals- Animals