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目的建立血链球菌感染性心内膜炎动物模型,为血链球菌相关毒力因子的研究奠定基础。方法健康獭兔40只,随机分为实验组(30只)和对照组(10只),兔颈总动脉插入导管,对心脏瓣膜造成机械性损伤。通过多通道生理信号采集系统监测血压以确定导管前端的正确位置,并留置导管于獭兔体内。术后24h,每只獭兔耳缘静脉注射109 CFU/ml血链球菌或中性磷酸盐缓冲液(PBS)1ml,分别于感染后3、4、5d观察獭兔存活情况。且自感染后3d开始,实验组每天取6只獭兔、对照组每天取3只处死,解剖心脏,观察心脏赘生物并称重,计数CFU。结果 109 CFU/ml的血链球菌感染后3、4、5d,实验动物心脏赘生物分别为0.21、0.21和0.23g,且与对照组0.03、0.03、0.14g比较差异有统计学意义(P<0.01)。同期实验组獭兔存活率分别为100.0%、62.5%和33.3%。结论成功建立了血链球菌感染性心内膜炎动物模型,为血链球菌相关毒力因子及致病机制研究奠定了基础。
Objective To establish an animal model of streptococcus sanguis infective endocarditis and lay the foundation for the study of the related virulence factors of Streptococcus sanguis. Methods Forty healthy Rex rabbits were randomly divided into experimental group (n = 30) and control group (n = 10). The rabbit common carotid artery was cannulated to cause mechanical damage to the heart valve. Blood pressure was monitored by a multi-channel physiological signal acquisition system to determine the correct position of the catheter tip and indwelling the catheter in the rex rabbit. At 24 hours after operation, each rex rabbit was intravenously injected with 1 ml of 109 CFU / ml Streptococcus sanguis or Neutral Phosphate Buffered Saline (PBS) to observe the survival of rex rabbits at 3, 4 and 5 days after infection respectively. Six days after the infection, six rex rabbits in the experimental group were sacrificed every day. Three rabbits in the control group were sacrificed every day. The hearts were dissected and their heart vegetation was observed. The CFU was counted. Results At 3,4 and 5 days after infection with 109 CFU / ml streptococcus spp, the experimental animals’ cardiac neoplasms were 0.21, 0.21 and 0.23 g, respectively, which were significantly different from those of the control group (0.03, 0.03 and 0.14 g, P < 0.01). The survival rates of rex rabbits in the experimental group were 100.0%, 62.5% and 33.3% respectively. Conclusion The animal model of streptococcus sanguis infective endocarditis has been successfully established, which lays the foundation for the study of related virulence factors and pathogenesis of Streptococcus sanguis.