Tomita M, Fukuuchi Y
Department of Neurology, School of Medicine, Keio University, Tokyo, Japan.
Acta Neurochir Suppl. 1996;66:32-9. doi: 10.1007/978-3-7091-9465-2_6.
The involvement of white blood cells in microvascular derangement as a cause of secondary brain damage following cerebral ischemia is reviewed. Relevant data from the literature are arranged in the chronological sequence of the microvascular derangement of the brain that occurs after cerebral arterial occlusion (as based on our own experimental observations). The inflammatory processes which appeared to be elicited by polymorphonuclear leukocytes (PMNL) in the ischemic region of the brain may begin with adhesion of PMNLs to endothelial cells, followed by blood-brain barrier disruption, transudation/exudation, edema, necrosis, and scar formation. Stimulated by cytokines released from damaged neurons and axons, two types of macrophages (ameboid and ramified) appear, increase in number in the ischemic lesion, and engulf the debris of dead neurons, degenerated axons. Further, macrophages may release cytokines which stimulate healing processes, such as astroglial proliferation and revascularization, and release neurotoxins which could gradually kill surviving neurons. Even under such circumstances, individual leukocytes/macrophages are well regulated by specific mediators/cytokines. An urgent task is thus to find ways of controlling these key mediators/cytokines to reduce the inflammatory process and the extent of neuronal death for attenuating the secondary brain damage, without altering their beneficial effects.
本文综述了白细胞在微血管紊乱中所起的作用，微血管紊乱是脑缺血后继发性脑损伤的一个原因。根据我们自己的实验观察，将文献中的相关数据按照大脑动脉闭塞后发生的脑微血管紊乱的时间顺序进行整理。在脑缺血区域，多形核白细胞（PMNL）引发的炎症过程可能始于PMNL与内皮细胞的黏附，随后是血脑屏障破坏、漏出/渗出、水肿、坏死和瘢痕形成。在受损神经元和轴突释放的细胞因子刺激下，出现两种类型的巨噬细胞（阿米巴样和分支状），在缺血性病变中数量增加，并吞噬死亡神经元和变性轴突的碎片。此外，巨噬细胞可能释放刺激愈合过程的细胞因子，如星形胶质细胞增殖和血管再生，还会释放可能逐渐杀死存活神经元的神经毒素。即便在这种情况下，单个白细胞/巨噬细胞仍受到特定介质/细胞因子的良好调控。因此，当务之急是找到控制这些关键介质/细胞因子的方法，以减少炎症过程和神经元死亡的程度，从而减轻继发性脑损伤，同时又不改变它们的有益作用。
