Intracortical hemorrhage injury in rats - Relationship between blood fractions and brain cell death

被引:157
作者
Xue, MZ [1 ]
Del Bigio, MR [1 ]
机构
[1] Univ Manitoba, Fac Med, Dept Pathol, Winnipeg, MB R3E 0W3, Canada
关键词
hematoma; inflammation; in situ nick-end labeling; lymphocytes; neutrophils;
D O I
10.1161/01.STR.31.7.1721
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Background and Purpose-Intracerebral hemorrhage is associated with stroke and head trauma. The purposes of this study were to investigate the effect of intracortical injections of autologous whole blood and blood components on inflammatory cell infiltration and brain cell death and to determine if nonhemorrhagic lesions differ in these respects. Methods-Eighty-seven adult rats were subjected to intracortical injections of autologous whole blood or allogeneic plasma, erythrocytes, leukocytes, "activated" leukocytes, and serum. Injections of saline or mineral oil were controls. Blood injections were compared with cortical freeze injury and pial devascularization. Rats were perfusion-fixed 48 hours after injection or lesioning. Eosinophilic neurons, TUNEL-positive cells, brain damage area, infiltrating neutrophils, and CD8a-immunoreactive lymphocytes were quantified. Results-Damage area, dying cells, and inflammatory infiltrate were significantly greater after autologous whole blood, leukocyte, and "activated" leukocyte injections than injection of other fractions. Conclusions-These results suggest that extravasated whole blood causes a greater degree of cortical cell death and inflammation than ischemic lesions of similar size. Leukocytes "activated" by systemic illness might exacerbate the injury. Secondary hemorrhagic phenomena suggest that the harmful effect is directed toward both brain cells and the vasculature. Further studies are required to delineate the mechanism(s).
引用
收藏
页码:1721 / 1727
页数:7
相关论文
共 60 条
[1]
Akopov S, 1996, CEREBROVAS BRAIN MET, V8, P11
[2]
Timing of early changes in brain trauma [J].
Anderson, RM ;
Opeskin, K .
AMERICAN JOURNAL OF FORENSIC MEDICINE AND PATHOLOGY, 1998, 19 (01) :1-9
[3]
[Anonymous], TECHNICAL MANUAL
[4]
The role of inflammation and cytokines in brain injury [J].
Arvin, B ;
Neville, LF ;
Barone, FC ;
Feuerstein, GZ .
NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS, 1996, 20 (03) :445-452
[5]
Chemokine and inflammatory cell response to hypoxia-ischemia in immature rats [J].
Bona, E ;
Andersson, AL ;
Blomgren, K ;
Gilland, E ;
Puka-Sundvall, M ;
Gustafson, K ;
Hagberg, H .
PEDIATRIC RESEARCH, 1999, 45 (04) :500-509
[6]
Bullock R, 1984, Neurol Res, V6, P184
[7]
A cautionary note on the use of the TUNEL stain to determine apoptosis [J].
CharriautMarlangue, C ;
BenAri, Y .
NEUROREPORT, 1995, 7 (01) :61-64
[8]
EXPERIMENTAL CEREBRAL EDEMA PRODUCED BY FOCAL FREEZING .1. ANATOMIC STUDY UTILIZING VITAL DYE TECHNIQUES [J].
CLASEN, RA ;
BOYD, D ;
COOKE, PM ;
RAIMONDI, AJ ;
PANDOLFI, S .
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY, 1962, 21 (04) :579-&
[9]
CLASEN RA, 1953, SURG GYNECOL OBSTET, V96, P605
[10]
Colbourne F, 1999, J NEUROSCI, V19, P4200