Alterations in blood vessels in X‐irradiated spinal cords of young rats

Administration of x‐rays (4000 r) to lumbar spinal cords of three‐day‐old rats caused a loss of neuroglia with an inhibition of myelinogenesis, neuronal damage and necrosis. In contrast, the loss of neuroglia following administration of 2000 r is temporary, with myelinogenesis occurring later than n...

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Veröffentlicht in:Anat. Rec., 163: 89-100(Jan. 1969) 163: 89-100(Jan. 1969), 1969-01, Vol.163 (1), p.89-99
1. Verfasser: Gilmore, Shirley Ann
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Sprache:eng
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Zusammenfassung:Administration of x‐rays (4000 r) to lumbar spinal cords of three‐day‐old rats caused a loss of neuroglia with an inhibition of myelinogenesis, neuronal damage and necrosis. In contrast, the loss of neuroglia following administration of 2000 r is temporary, with myelinogenesis occurring later than normal. Preliminary observations suggested that differences in vascular responses to these two amounts of x‐rays might account for these differing fates of the spinal cords; therefore, this investigation was designed to study further the reactions of the intramedullary vessels. Rats, irradiated when three days of age, were killed 1 to 27 days later. Some were killed by perfusion with Monolite Fast Blue BNVSA Paste, a substance retained in the vessels and readily visualized on microscopic examination. The remaining rats were decapitated, and spinal cords were stained by Gomori's method for alkaline phosphatase. The earliest consistent alteration, a decreased number of vessels, was noted seven days following irradiation with either dose. Rats receiving 4000 r had marked losses of blood vessels, vasodilatation and necrosis by 15 days post‐irradiation; whereas, a decreased number of vessels was the only change noted in rats irradiated with 2000 r. Alterations in rats receiving 4000 r remained the same or became more severe throughout the study; spinal cords in rats receiving 2000 r returned to normal. These vascular alterations correlate well with the changes in other spinal cord components described previously by this investigator.
ISSN:0003-276X
1097-0185
DOI:10.1002/ar.1091630111