Complement depletion improves neurological function in cerebral ischemia

被引:74
作者
Vasthare, US
Barone, FC
Sarau, HM
Rosenwasser, RH
DiMartino, M
Young, WF
Tuma, RF [1 ]
机构
[1] Temple Univ, Dept Physiol, Sch Med, Philadelphia, PA 19140 USA
[2] Temple Univ, Sch Med, Dept Neurosurg, Philadelphia, PA 19122 USA
[3] SmithKline Beecham Pharmaceut, Dept Pharmacol, King Of Prussia, PA 19406 USA
关键词
complement system; evoked potentials; transient forebrain ischemia; neutrophils; myeloperoxidase; cobra venom factor;
D O I
10.1016/S0361-9230(97)00408-5
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The contribution of the complement system to the exacerbation of cerebral ischemia/reperfusion injury was studied by comparing a group of rats with normal complement levels to another group that was complement depleted by cobra venom factor (CVF), The magnitude of reactive hyperemia was significantly greater in the complement depleted animals, There was also better preservation of somatosensory evoked potentials (SSEPs) in the complement depleted animals, These differences were not associated with changes in leukocyte infiltration as evidenced by myeloperoxidase and Leukotriene B-4 activity. These data demonstrate that depleting the complement system can improve flow and outcome following cerebral ischemia with reperfusion. (C) 1998 Elsevier Science Inc.
引用
收藏
页码:413 / 419
页数:7
相关论文
共 56 条
[1]   REPERFUSION INCREASES NEUTROPHILS AND LEUKOTRIENE-B4 RECEPTOR-BINDING IN RAT FOCAL ISCHEMIA [J].
BARONE, FC ;
SCHMIDT, DB ;
HILLEGASS, LM ;
PRICE, WJ ;
WHITE, RF ;
FEUERSTEIN, GZ ;
CLARK, RK ;
LEE, EV ;
GRISWOLD, DE ;
SARAU, HM .
STROKE, 1992, 23 (09) :1337-1347
[2]   POLYMORPHONUCLEAR LEUKOCYTE INFILTRATION INTO CEREBRAL FOCAL ISCHEMIC TISSUE - MYELOPEROXIDASE ACTIVITY ASSAY AND HISTOLOGIC VERIFICATION [J].
BARONE, FC ;
HILLEGASS, LM ;
PRICE, WJ ;
WHITE, RF ;
LEE, EV ;
FEUERSTEIN, GZ ;
SARAU, HM ;
CLARK, RK ;
GRISWOLD, DE .
JOURNAL OF NEUROSCIENCE RESEARCH, 1991, 29 (03) :336-345
[3]   THE ROLE OF NEUTROPHILS AND PLATELETS IN A RABBIT MODEL OF THROMBOEMBOLIC STROKE [J].
BEDNAR, MM ;
RAYMOND, S ;
MCAULIFFE, T ;
LODGE, PA ;
GROSS, CE .
STROKE, 1991, 22 (01) :44-50
[4]  
Bednar MM, 1996, NEUROL RES, V18, P171
[5]   MONOCLONAL-ANTIBODY TO THE ICAM-1 ADHESION SITE REDUCES NEUROLOGICAL DAMAGE IN A RABBIT CEREBRAL EMBOLISM STROKE MODEL [J].
BOWES, MP ;
ZIVIN, JA ;
ROTHLEIN, R .
EXPERIMENTAL NEUROLOGY, 1993, 119 (02) :215-219
[6]   MEASUREMENT OF CUTANEOUS INFLAMMATION - ESTIMATION OF NEUTROPHIL CONTENT WITH AN ENZYME MARKER [J].
BRADLEY, PP ;
PRIEBAT, DA ;
CHRISTENSEN, RD ;
ROTHSTEIN, G .
JOURNAL OF INVESTIGATIVE DERMATOLOGY, 1982, 78 (03) :206-209
[7]  
CATTELL V, 1979, BRIT J EXP PATHOL, V60, P201
[8]  
CHEN H, 1992, NEUROSCI RES COMMUN, V11, P93
[9]   DEVELOPMENT OF TISSUE-DAMAGE, INFLAMMATION AND RESOLUTION FOLLOWING STROKE - AN IMMUNOHISTOCHEMICAL AND QUANTITATIVE PLANIMETRIC STUDY [J].
CLARK, RK ;
LEE, EV ;
FISH, CJ ;
WHITE, RF ;
PRICE, WJ ;
JONAK, ZL ;
FEUERSTEIN, GZ ;
BARONE, FC .
BRAIN RESEARCH BULLETIN, 1993, 31 (05) :565-572
[10]   REDUCTION OF CENTRAL-NERVOUS-SYSTEM ISCHEMIC-INJURY BY MONOCLONAL-ANTIBODY TO INTERCELLULAR-ADHESION MOLECULE [J].
CLARK, WM ;
MADDEN, KP ;
ROTHLEIN, R ;
ZIVIN, JA .
JOURNAL OF NEUROSURGERY, 1991, 75 (04) :623-627