NEUTROPHIL ACTIVATION IN ACUTE HUMAN CENTRAL NERVOUS SYSTEM INJURY

中性粒细胞活化加重脑损伤的假设 急性中风目前已被广泛接受。 但 中性粒细胞活化与脑缺血事件的时间关系 临床状态不明确。 因此，本研究旨在 用鲁米诺依赖的技术检测人中性粒细胞活化 急性温和性和出血性中风的化学发光。 患者 （空白，n = 18;出血，n = 16）在6个月内进入本研究 时间的冲击。 这些结果与其他临床中心进行了比较。 神经系统损伤：蛛网膜下腔出血（n = 11）、脊柱创伤 单纯闭合性颅脑损伤19例。 所有受试者均被采样 在急诊室就诊时以及0.5、1、2、3、4和5天 在事件之后。 通过鲁米诺测定的神经元活化- 依赖性化学发光，在发病后第1天明显， 轻度脑卒中组（P <0.05），虽然这种趋势没有得到证实 治疗出血性中风 患有闭合性头部损伤的患者 显示出更大的初始中性粒细胞活化， 在第0.5天（p-9.91）和第1天（p = 0.05）显著低于基线。 没有 脊柱创伤组和 蛛网膜下腔出血这些结果支持中性粒细胞 在各种中枢神经系统损伤期间激活，并提供 考虑针对短暂性的药物治疗的时间框架 抑制中性粒细胞功能。

The hypothesis that neutrophil activation exacerbates brain injury in acute stroke is currently receiving wide acceptance. However, the temporal relationship of neutrophil activation to the ischemic event in clinical states is not clear. Therefore, this study was undertaken to examine human neutrophil activation by the technique of luminol-dependent chemiluminescence in both acute bland and hemorrhagic stroke. Patients (bland, n-18; hemorrhagic, n=16) were entered into this study within six hours of the ictus. These results were compared to other clinical central nervous system insults: subarachnoid hemorrhage (n=11), spinal trauma (n=9) and isolated closed heady injury (n=19). All subjects were sampled upon presentation to the emergency room and 0.5, 1, 2, 3, 4 and 5 days following the event. Neutrophil activation, as determined by luminol- dependent chemiluminescence, was evident at day 1 following the ictus in the bland stroke group (p<0.05), although this trend was not demonstrated for hemorrhagic stroke. Patients suffering a closed head injury demonstrated greater initial neutrophil activation with values being significantly lower than baseline at days 0.5 (p-9.91) and 1 (p=0.05). No significant change was demonstrated for the groups with spinal trauma or subarachnoid hemorrhage. These results support a role for neutrophil activation during various central nervous system insults and provide a temporal framework for considering drug therapy directed at transient suppression of neutrophil function.