Toky V, Sharma S, Bramhne H G, Chhibber S
Department of Microbiology, Panjab University, 160 014 Chandigarh, India.
Folia Microbiol (Praha). 2005;50(2):167-71. doi: 10.1007/BF02931467.
In a fibrin-clot model of sepsis, developed in mice, treatment with the antibiotics ceftazidime (Cfz) and ofloxacin (Ofl) caused significant (p < 0.01) release of endotoxin and TNF-alpha after 4.5 h when compared with control (untreated) and amikacin (Ami) treated group. Except for control group, the level of bacteremia declined in all three antibiotic-treated groups. The results suggest that antibiotic therapy, irrespective of the agent used, results in an increase in endotoxin levels in vivo. The amount of endotoxin liberated by Ami was much smaller than with Cfz and Ofl therapy, which makes it an appropriate agent for the treatment of sepsis. An increase in the level of TNF-alpha along with endotoxin is suggestive of increased inflammatory response.
在小鼠中建立的脓毒症纤维蛋白凝块模型中,与对照组(未治疗)和阿米卡星(Ami)治疗组相比,用抗生素头孢他啶(Cfz)和氧氟沙星(Ofl)治疗4.5小时后,内毒素和肿瘤坏死因子-α(TNF-α)出现显著(p < 0.01)释放。除对照组外,所有三个抗生素治疗组的菌血症水平均下降。结果表明,无论使用何种药物,抗生素治疗都会导致体内内毒素水平升高。阿米卡星释放的内毒素量远低于头孢他啶和氧氟沙星治疗组,这使其成为治疗脓毒症的合适药物。TNF-α水平与内毒素一起升高表明炎症反应增强。