Nikolić S
Dr. Kosta Todorović Institute of Infectious and Tropical Diseases, University Clinical Centre, Belgrade.
Srp Arh Celok Lek. 1992 Nov-Dec;120(11-12):353-5.
Pathophysiologic disorders in bacterial meningitis and their influence on the course and prognosis of the disease are analysed. Deterioration of the CNS is due to inflammatory response of the host combined with other pathophysiological disorders. Inflammatory response in the subarachnoid space is the most intensive, but the most deleterious, as well, in the first several hours of antibiotic therapy when bacterial disintegration ensues. Fragments of the cell wall and endotoxin are very active components, independent of the presence of living bacteria in the subarachnoid space. Each microorganism induces different inflammatory response, and the course of the disease is, therefore, also different. Bacterial disintegration reta and release of the components are determined by the intensity of the inflammatory response in the subarachnoid space. Which, in turn, determine the degree of tissue damage. Bacterial products stimulate release of inflammatory mediators--cytokines from macrophages and other sources. Local production of cytokines from astrocytes and macroglial cells (macrophage equivalents in the CNS) is the first stage in development of the inflammatory response and tissue destruction. Cytokines induce damage of the CNS by attracting the inflammatory cells and by releasing superoxide anions inducing arachidonic acid metabolism and production of vasoactive metabolites of arachidonic acid which result in damage of blood-brain barrier, having, therefore, a direct cytotoxic effect. Consequences of these pathophysiologic disorders are cerebral oedema and elevated intracranial pressure. Current concepts of antiinflammatory therapy are, in the light of pathophysiological events in the CNS, directed to interruption of cytokine activation (steroids), prevention of production of vasoactive arachidonic acid metabolites (non-steroidal agents), and prevention of leukocyte transfer into the subarachnoid space (antileukocyte, anti-integrin antibodies).
分析了细菌性脑膜炎的病理生理紊乱及其对疾病进程和预后的影响。中枢神经系统的恶化是由于宿主的炎症反应以及其他病理生理紊乱所致。蛛网膜下腔的炎症反应最为强烈，但在抗生素治疗的最初几个小时内，当细菌解体时，也是最有害的。细胞壁碎片和内毒素是非常活跃的成分，与蛛网膜下腔中活细菌的存在无关。每种微生物诱导不同的炎症反应，因此疾病进程也不同。细菌解体的速度和成分的释放取决于蛛网膜下腔炎症反应的强度，而这又反过来决定了组织损伤的程度。细菌产物刺激炎症介质——巨噬细胞和其他来源的细胞因子的释放。星形胶质细胞和大胶质细胞（中枢神经系统中的巨噬细胞等效物）局部产生细胞因子是炎症反应和组织破坏发展的第一阶段。细胞因子通过吸引炎症细胞并释放超氧阴离子诱导花生四烯酸代谢和花生四烯酸血管活性代谢产物的产生，从而导致血脑屏障受损，因此具有直接的细胞毒性作用。这些病理生理紊乱的后果是脑水肿和颅内压升高。根据中枢神经系统中的病理生理事件，当前的抗炎治疗概念旨在中断细胞因子激活（类固醇）、预防血管活性花生四烯酸代谢产物的产生（非甾体类药物）以及预防白细胞转移到蛛网膜下腔（抗白细胞、抗整合素抗体）。
