Post-ischemic hypothermia delayed neutrophil accumulation and microglial activation following transient focal ischemia in rats
Post-ischemic hypothermia delayed neutrophil accumulation and microglial activation following transient focal ischemia in rats
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DOI：
10.1016/s0165-5728(00)00211-3
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发表时间：
2000-09-22
影响因子：
3.3
通讯作者：
Kawase, T
中科院分区：
文献类型：
--
作者：
Inamasu, J;Suga, S;Kawase, T
缺血后，炎症已被证明参与组织损伤的进展。缺血内低温已被证明可以减弱中性粒细胞和小胶质细胞的不良活动。我们研究了中性粒细胞的积累和/或小胶质细胞的激活是否在短暂性局灶性脑缺血后的缺血后低温中减弱。缺血1小时后，免疫组化评价中性粒细胞聚集和小胶质细胞活化。在缺血/再灌注后1、2、3、5和7天比较梗塞面积百分比。在低温下，中性粒细胞聚集延迟，但不减弱。常温下，缺血后2d达高峰。在低温下，峰值移至3天。同样，在低温下，小胶质细胞的激活也被延迟。再灌注后1天和2天的梗死面积比较显示，低温具有显著的保护作用。然而，低温在3天及以后未能表现出显着的保护作用。这些结果表明，延迟的中性粒细胞聚集和小胶质细胞活化可能是缺血后低温失去持久保护的原因。(C)2000爱思唯尔科技有限公司。保留所有权利。
Following ischemia, inflammation has been demonstrated to be involved in the progression of the tissue damage. Intra-ischemic hypothermia has been shown to attenuate the adverse activities of neutrophils and microglia. We investigated whether neutrophil accumulation and/or microglial activation is attenuated in post-ischemic hypothermia following transient focal ischemia in rats. After 1 h of ischemia, the neutrophil accumulation and the microglial activation was evaluated immunohistochemically. Percent infarct area was compared at 1, 2, 3, 5, and 7 days after ischemia/reperfusion. In hypothermia, the neutrophil accumulation was delayed but not attenuated. In normothermia, the accumulation reached the peak at 2 days after ischemia. The peak shifted to 3 days in hypothermia. Similarly; the microglial activation was delayed in hypothermia. Comparison of the infarct area showed significant protection by hypothermia at 1 and 2 days after reperfusion. However, hypothermia failed to show significant protection after 3 days and later. These results show that the delayed neutrophil accumulation and the microglial activation can be responsible for the loss of persistent protection in post-ischemic hypothermia. (C) 2000 Elsevier Science B.V. All rights reserved.