EFFECT OF RECIRCULATION ON EXACERBATION OF ISCHEMIC VASCULAR-LESIONS IN RAT-BRAIN

被引:62
作者
NISHIGAYA, K
YOSHIDA, Y
SASUGA, M
NUKUI, H
OONEDA, G
机构
[1] YAMANASHI MED COLL,DEPT PATHOL,1110 SHIMOKATO,YAMANASHI 40938,JAPAN
[2] INST GERIAT,MAEBASHI,JAPAN
[3] YAMANASHI MED COLL,DEPT NEUROSURG,YAMANASHI 40938,JAPAN
关键词
BRAIN EDEMA; MICROCIRCULATION; REPERFUSION; RATS;
D O I
10.1161/01.STR.22.5.635
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Using electron microscopy, we investigated the small arteries and veins in ischemic lesions induced by occlusion of the ostium of the middle cerebral artery in 42 rats. We observed endothelial denudation in the small arteries of rats receiving occlusion for > 6 hours. When the occluding cylinder was removed to allow for reperfusion, however, 2 hours of occlusion was sufficient for endothelial denudation to occur. Medial smooth muscle cells seemed to be more vulnerable to ischemia than endothelial cells because ultrastructural changes in the former cells preceded endothelial denudation. Moreover, endothelial denudation definitely exacerbated vascular changes so that medial necrosis appeared to be complete beneath the denuded areas, allowing erythrocytes, platelets, and exogenous tracers to penetrate into the cytoplasm of smooth muscle cells. These arterial lesions seemed to be repaired 10 days after removal of the occluding cylinder following 2 hours of occlusion. On the other hand, small veins in the ischemic lesion did not show endothelial denudation or medial necrosis. Our study suggests that arterial changes in ischemic lesions play a role in exacerbating the brain edema caused by recirculation after ischemia.
引用
收藏
页码:635 / 642
页数:8
相关论文
共 18 条
[1]  
AMES A, 1968, AM J PATHOL, V52, P437
[2]  
CHIANG J, 1968, AM J PATHOL, V52, P455
[3]   MORPHOLOGICAL CONSEQUENCES OF EARLY REPERFUSION FOLLOWING THROMBOTIC OR MECHANICAL OCCLUSION OF THE RAT MIDDLE CEREBRAL-ARTERY [J].
DIETRICH, WD ;
NAKAYAMA, H ;
WATSON, BD ;
KANEMITSU, H .
ACTA NEUROPATHOLOGICA, 1989, 78 (06) :605-614
[4]   CEREBRAL ENDOTHELIAL MICROVILLI - FORMATION FOLLOWING GLOBAL FOREBRAIN ISCHEMIA [J].
DIETRICH, WD ;
BUSTO, R ;
GINSBERG, MD .
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY, 1984, 43 (01) :72-83
[5]   PERIVASCULAR HEMORRHAGIC LESIONS IN TEMPORAL CORTEX FOLLOWING CEREBRAL INFARCTION (A MORPHOLOGICAL STUDY) [J].
DODSON, RF ;
KAWAMURA, Y .
EXPERIMENTAL AND MOLECULAR PATHOLOGY, 1974, 20 (01) :24-32
[6]   ULTRASTRUCTURE MICROVASCULATURE IN EXPERIMENTAL CEREBRAL INFARCTION [J].
GARCIA, JH ;
COX, JV ;
HUDGINS, WR .
ACTA NEUROPATHOLOGICA, 1971, 18 (04) :273-&
[7]   EFFECT OF HYPERTENSION ON BLOOD-BRAIN-BARRIER CHANGE AFTER RESTORATION OF BLOOD-FLOW IN POST-ISCHEMIC GERBIL BRAINS - AN ELECTRON-MICROSCOPIC STUDY [J].
ITO, U ;
OHNO, K ;
YAMAGUCHI, T ;
TAKEI, H ;
TOMITA, H ;
INABA, Y .
STROKE, 1980, 11 (06) :606-611
[8]   THE DISSOCIATION OF CEREBRAL BLOOD-FLOW, METABOLISM, AND FUNCTION IN THE EARLY STAGES OF DEVELOPING CEREBRAL INFARCTION [J].
KOGURE, K ;
BUSTO, R ;
SCHWARTZMAN, RJ ;
SCHEINBERG, P .
ANNALS OF NEUROLOGY, 1980, 8 (03) :278-290
[9]  
Koizumi J., 1986, J N J STROK, V8, P1, DOI DOI 10.3995/JSTROKE.8.1
[10]  
KOIZUMI Z, 1989, JPN J STROKE, V11, P11