Stroke, Vol 21, 1722-1726, Copyright © 1990 by American Heart Association
N Yamazoe, N Hashimoto, H Kikuchi and F Hazama
In an attempt to clarify the developmental mechanism of cerebral aneurysms,
we studied the elastic skeleton of experimentally induced cerebral
aneurysms in rats under scanning electron microscopy after hot formic acid
extraction followed by freeze-drying. We produced cerebral aneurysms in 19
rats by unilaterally ligating the common carotid artery, inducing renal
hypertension, and feeding beta- aminopropionitrile fumarate. The first
noted change was the loss of folds protruding from the internal elastic
lamina. Morphologic changes of the internal elastic lamina, considered to
be primarily responsible for aneurysmal formation, occurred after the loss
or disintegration of the elastic skeleton of first the intima, then the
media. In large aneurysms with thick domes, we found proliferation of
elastic lamellae that may reduce the risk of rupture. It seems probable
that the complex elastic skeleton of the arterial wall may account for the
mechanical properties of the artery and that growth of an aneurysm occurs
due to disintegration of the elastic skeleton and not simply to rupture of
the internal elastic lamina. We believe that such changes in the elastic
skeleton are a property of the functional state of the cells that produce
elastin.
ARTICLES
Elastic skeleton of intracranial cerebral aneurysms in rats
Department of Neurosurgery, Kyoto University Medical School and Hospital, Japan.
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