Acute inflammatory reaction following experimental intracerebral hemorrhage in rat
Acute inflammatory reaction following experimental intracerebral hemorrhage in rat
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DOI：
10.1016/s0006-8993(00)02427-6
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发表时间：
2000-07-14
期刊：
影响因子：
2.9
通讯作者：
Keep, RF
中科院分区：
文献类型：
--
作者：
Gong, C;Hoff, JT;Keep, RF
先前对脑出血 (ICH) 的研究表明，脑水肿在最初 24 小时内逐渐加重，并在数天内保持升高状态。继发性脑损伤和水肿形成的原因尚不清楚。我们推测脑出血后血液中释放的炎症介质可能导致继发性脑损伤和水肿形成。本研究调查大鼠脑出血后是否、何时以及何地发生炎症。对照组及右侧基底节区注射100μl自体血后第1、3、7、10天进行多形核白细胞标记物（髓过氧化物酶，MPO）、小胶质细胞标记物（OX42）和细胞内粘附分子-1（ICAM-1）的免疫细胞化学检查。双标记免疫组化用于鉴定ICAM-1阳性细胞。结果表明，ICH后血凝块内及其周围发生炎症反应，其特征是中性粒细胞和巨噬细胞浸润以及小胶质细胞激活。在凝块附近的血管以及同侧半球的激活的小胶质细胞和神经元中观察到 ICAM-1 免疫反应性。目前的研究表明，六六六后大脑中出现炎症反应。浸润白细胞和活化的小胶质细胞可能释放细胞毒性介质，导致继发性脑损伤。 (C) 2000 Elsevier Science B.V. 保留所有权利。
Previous studies on intracerebral hemorrhage (ICH) indicate that brain edema increases progressively in the first 24 h and remains elevated for several days. The cause of secondary brain injury and edema formation is uncertain. We hypothesized that inflammatory mediators released from the blood after cerebral hemorrhage might cause secondary brain injury and edema formation. This study investigates if, when and where inflammation occurs after ICH in rat. Immunocytochemistry for polymorphonuclear leukocyte marker (myeloperoxidase, MPO), microglia marker (OX42) and intracellular adhesion molecule-1 (ICAM-1) was performed in control, and 1, 3, 7 and 10 days after the injection of 100 mu l autologous blood in the right basal ganglia. Double labeling immunohistochemistry was used to identify ICAM-1 positive cells. The results show that an inflammatory response occurred in and around the blood clot after ICH, characterized by the infiltration of neutrophils and macrophages as well as activation of microglia. ICAM-1 immunoreactivity was observed in blood vessels adjacent to the clot, as well as in activated microglia and neurons in the ipsilateral hemisphere. The present study demonstrates there is an inflammatory response in the brain after HCH. Infiltrating leukocytes and activated microglia may release cytotoxic mediators contributing to secondary brain injury. (C) 2000 Elsevier Science B.V. All rights reserved.