Extracellular superoxide dismutase deficiency worsens outcome from focal cerebral ischemia in the mouse

被引：78

作者：

Sheng, HX

Brady, TC

Pearlstein, RD

Crapo, JD

Warner, DS ^{[1
]}

机构：

[1] Duke Univ, Med Ctr, Dept Anesthesiol, Durham, NC 27710 USA

[2] Duke Univ, Med Ctr, Dept Pathol, Durham, NC 27710 USA

[3] Duke Univ, Med Ctr, Dept Surg, Durham, NC 27710 USA

[4] Natl Jewish Ctr Immunol & Resp Med, Dept Med, Denver, CO 80206 USA

来源：

NEUROSCIENCE LETTERS | 1999年 / 267卷 / 01期

关键词：

extracellular superoxide dismutase; brain; ischemia; mouse;

D O I：

10.1016/S0304-3940(99)00316-X

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

The role of endogenous extracellular superoxide dismutase (EC-SOD) was examined in a murine model of transient focal cerebral ischemia. Homozygous EC-SOD deficient (EC-SOD-/-; n = 18) and wild type (EC-SOD+/+; n = 19) littermates were anesthetized with halothane and subjected to 50 min of intraluminal middle cerebral artery occlusion with pericranial temperature maintained at 37.0 degrees C. After 24 h of reperfusion, resultant hemiparesis and cerebral infarct size were measured. Total infarct volume was 81% greater (P = 0.03) and hemiparesis was more severe (P = 0.01) in EC-SOD-/- versus EC-SOD+/+ mice. The worsened ischemic outcome observed in EC-SOD-/- mice is consistent with prior work which found transgenic EC-SOD overexpressing mice to exhibit enhanced tolerance to focal ischemia. The results suggest that endogenous antioxidant activity in the extracellular compartment plays an important role in the histologic/neurologic response to focal cerebral ischemia. (C) 1999 Elsevier Science Ireland Ltd. All rights reserved.

引用

页码：13 / 16

页数：4

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