Leib S L, Kim Y S, Black S M, Tureen J H, Täuber M G
Infectious Diseases Laboratory, San Francisco General Hospital, University of California, USA.
J Infect Dis. 1998 Mar;177(3):692-700. doi: 10.1086/514226.
This study explored the role of inducible nitric oxide (NO) synthase (iNOS) in an infant rat model of group B streptococcal meningitis. Brain iNOS activity increased during meningitis (P < .001), and iNOS was detected by immunocytochemistry in the walls of meningeal vessels and cells of the cerebrospinal fluid (CSF) inflammation. Animals treated with iNOS inhibitor aminoguanidine (AG; 130 mg/kg every 8 h) had reduced NO production (P < .05), higher CSF bacterial titers (P < .05), and increased incidence of seizures (P < .01) compared with untreated infected animals. AG also increased areas of severe hypoperfusion in the cortex (31% +/- 14% in controls vs. 56% +/- 16% in AG; P < .01) and the extent of cortical neuronal injury, both when administered at the time of infection (P < .05) and in established meningitis (P < .02). Thus, NO produced by iNOS may be beneficial in this model of experimental meningitis by reducing cerebral ischemia.
本研究探讨了诱导型一氧化氮(NO)合酶(iNOS)在B族链球菌性脑膜炎幼鼠模型中的作用。脑膜炎期间脑iNOS活性增加(P <.001),通过免疫细胞化学在脑膜血管壁和脑脊液(CSF)炎症细胞中检测到iNOS。与未治疗的感染动物相比,用iNOS抑制剂氨基胍(AG;每8小时130 mg/kg)治疗的动物NO产生减少(P <.05),脑脊液细菌滴度更高(P <.05),癫痫发作发生率增加(P <.01)。AG还增加了皮质严重灌注不足的面积(对照组为31%±14%,AG组为56%±16%;P <.01)以及皮质神经元损伤的程度,无论是在感染时给予AG(P <.05)还是在已确诊的脑膜炎中给予AG(P <.02)。因此,iNOS产生的NO可能通过减少脑缺血在该实验性脑膜炎模型中发挥有益作用。