Protective effect of C1 esterase inhibitor on reperfusion injury in the rat middle cerebral artery occlusion model

被引:57
作者
Akita, N [1 ]
Nakase, H [1 ]
Kaido, T [1 ]
Kanemoto, Y [1 ]
Sakaki, T [1 ]
机构
[1] Nara Med Univ, Dept Neurosurg, Kashihara, Nara 6348522, Japan
关键词
C1 esterase inhibitor; complement; leukocytes; myeloperoxidase; reperfusion injury;
D O I
10.1227/01.NEU.0000043710.61233.B4
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
OBJECTIVE: The complement system is thought to play a major role in initiating some of the inflammatory events that occur during reperfusion injury. The aim of this study was to assess the effects of Cl esterase inhibitor (C1-INH) on ischemic injury in the rat model of middle cerebral artery suture occlusion and reperfusion. METHODS: Thirty-six male Wistar rats were used. Intraluminal middle cerebral artery occlusion was performed for 60 minutes. just before reperfusion, C1-INH (50 international units/kg) (C1-INH group, In = 19) or saline solution (control group, n = 17) was administered. Physiological parameters (arterial blood gas values, mean arterial blood pressure, and heart rate) and local cerebral blood flow were recorded during the experiment. Forty-eight hours after reperfusion, all rats were killed, and assessments of leukocyte infiltration with a myeloperoxidase activity assay and histological analyses with 2,3,5-triphenyl tetrazolium chloride staining were performed. RESULTS: The physiological parameters and local cerebral blood flow values were not significantly different in the two groups. The infarction volume was significantly smaller and the myeloperoxidase activity was significantly lower in the C1-INH group (84.9 +/- 69.1 mm(3) and 0.40 +/- 0.29 units/g, respectively) than in the control group (202.3 +/- 98.3 mm(3) and 1.41 +/- 0.44 units/g, respectively) (P < 0.01). Myeloperoxidase activities were strongly correlated with infarction volumes (r = 0.73, P < 0.01). CONCLUSION: The results of this study indicated that C1-INH reduced polymorphonuclear leukocyte accumulation and neuronal damage in focal ischemia and reperfusion.
引用
收藏
页码:395 / 400
页数:6
相关论文
共 30 条
[1]
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
[2]
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
[3]
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
[4]
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
[5]
CARDIOPROTECTIVE EFFECTS OF A C1 ESTERASE INHIBITOR IN MYOCARDIAL-ISCHEMIA AND REPERFUSION [J].
BUERKE, M ;
MUROHARA, T ;
LEFER, AM .
CIRCULATION, 1995, 91 (02) :393-402
[6]
CHIANG J, 1968, AM J PATHOL, V52, P455
[7]
NEUTROPHIL ACCUMULATION AFTER TRAUMATIC BRAIN INJURY IN RATS - COMPARISON OF WEIGHT DROP AND CONTROLLED CORTICAL IMPACT MODELS [J].
CLARK, RSB ;
SCHIDING, JK ;
KACZOROWSKI, SL ;
MARION, DW ;
KOCHANEK, PM .
JOURNAL OF NEUROTRAUMA, 1994, 11 (05) :499-506
[8]
In stroke, complement will get you nowhere [J].
del Zoppo, GJ .
NATURE MEDICINE, 1999, 5 (09) :995-996
[9]
POLYMORPHONUCLEAR LEUKOCYTES OCCLUDE CAPILLARIES FOLLOWING MIDDLE CEREBRAL-ARTERY OCCLUSION AND REPERFUSION IN BABOONS [J].
DELZOPPO, GJ ;
SCHMIDSCHONBEIN, GW ;
MORI, E ;
COPELAND, BR ;
CHANG, CM .
STROKE, 1991, 22 (10) :1276-1283
[10]
CEREBRAL INFARCTION - EVOLUTION OF HISTOPATHOLOGICAL CHANGES AFTER OCCLUSION OF A MIDDLE CEREBRAL-ARTERY IN PRIMATES [J].
GARCIA, JH ;
KAMIJYO, Y .
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY, 1974, 33 (03) :408-421