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机构地区:[1]中南大学湘雅第二医院神经外科,湖南长沙410011
出 处:《创伤外科杂志》2006年第5期394-397,F0004,共5页Journal of Traumatic Surgery
摘 要:目的 研究大鼠颅脑损伤后脑内中性粒细胞聚集、浸润的时间过程,并探讨与继发性脑损伤的关系。方法 采用改进的Feeney法复制大鼠颅脑损伤模型,将32只健康雄性SD大鼠随机分为假致伤组和致伤组,致伤组于伤后7个不同时相点断头、取脑,行髓过氧化物酶(MPO)活性测定和HE染色。结果 致伤组大鼠脑组织MPO活性表达从伤后3小时开始出现,伤后12~48小时达到高峰,但伤后72小时开始下降,伤后7天降至假致伤组水平。随着中性粒细胞的出现、聚集及浸润,此现象逐渐明显,损伤灶脑组织病理改变加重。结论 颅脑损伤后脑内中性粒细胞的聚集和浸润是颅脑损伤后脑内炎症反应的主要表现,其在继发性脑损伤的病理过程中可能起着重要的作用。Objective To study the course of polymorphonuclear leukocyte ( PMNL) infiltration into the injured parenchyma after traumatic brain injury (TBI ) , also to evaluate the contributions of inflammatory response to the secondary brain injury (SBI). Methods Using the Feeney's free-falling weight model,32 male Sprague-Dawley ( SD ) rats were randomly separated into sham-injured groups and injured groups. The damaged region of brain were removed in different time phases, stained with hematoxylin and eosin ( HE ) to evaluate the histopathologic changes. Myeloperoxidase (MPO) activity was measured to study the duration of PMNL aggregation infiltration in the brain regions post-trauma. Results PMNL aggregation and infiltration in injured brain progressively increased following histopathologic exacerbation. MPO activity appeared in injured brain from 3 hours post-trauma,reached its peak value at 12-48 hours,reduced at 72 hours and resolved by 7 days after trauma. Conclusion A local inflammatory response was initiated immediately following TBI and is characterized by the accumulation and infiltration of PMNL,and inflammation may play an important role in the pathogenesis of secondary cerebral injury after traumatic brain injury.
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