DSpace university logo mark
Japanese | English 

NAOSITE : Nagasaki University's Academic Output SITE > 030 医学部 > 030 紀要 > Acta Medica Nagasakiensia > Volume 16, No. 1-2 >

Ultrastructural Studies of Experimental Arteriosclerosis Arterial Lesions Produced by Hemodynamic Change

ファイル 記述 サイズフォーマット
acta16_01_04_t.pdf7.22 MBAdobe PDF本文ファイル

タイトル: Ultrastructural Studies of Experimental Arteriosclerosis Arterial Lesions Produced by Hemodynamic Change
著者: Taura, Seiya
著者(別表記) : 田浦, 晴也
発行日: 1971年10月25日
引用: Acta medica Nagasakiensia. 1971, 16(1-2), p.38-58
抄録: Sudden change of blood stream is considered as one of the pathological factors of arteriosclerosis. Rabbits were subjected to the dissection of the bilateral common carotid arteries and were sacrificed at certain time intervals. Observation was made for the behavior of the mural cells of the arteries in the cerebral basilar arterial system. One week after the operation, some media smooth muscle cells beneath the internal elastic lamina became irregular shape, and two weeks after the operation, they were even advanced to the state of coagulation necrosis showing marked increase of electron density in the cytoplasm. About the same time, the subendothelial space was immigrated by the media smooth muscle cells through the fenestrae of the internal elastic lamina, and thus intimal thickening was produced. At the advanced stage of experiment, medial thinning due to destruction and absorption of media smooth muscle cells became remarkable, but intimal thickening was not greatly intensified. As a result, the arteries showed dilatative lesion rather than stenosis of intimal thickening. The presence of a peculiar structure called Willis' ring in the cerebral basilar arterial system could not neglect as another cause of the dilatative lesion.
URI: http://hdl.handle.net/10069/15568
ISSN: 00016055
資料タイプ: Departmental Bulletin Paper
原稿種類: publisher
出現コレクション:Volume 16, No. 1-2

引用URI : http://hdl.handle.net/10069/15568



Valid XHTML 1.0! Copyright © 2006-2015 長崎大学附属図書館 - お問い合わせ Powerd by DSpace