Rink R D, Kaelin C R, Raque G, Trachtenberg L S, Fry D E
Lab Invest. 1982 Mar;46(3):282-7.
To test for synergy between a facultative and anaerobic bacterium and the role hepatic hypoxia may have in its development, rats were subjected to intravascular infusion of 10(8) Escherichia coli, 10(9) Bacteroides fragilis, or a combination of both. Acute effects were evaluated by selected 6-hour measurements, including hepatic pO2, and longer range effects by liver cultures and histology in rats surviving 7 days. During the acute period, systemic arterial pressure and pO2 in bacteremic groups did not differ from saline-infused controls. However, hepatic oxygen supply was significantly reduced in E. coli rats and those given the combined bacteria (mean hepatic pO2 less than 10 mm. Hg versus 20.8 mm. Hg in controls). Significant increases of plasma lactate and pulse rate were also recorded. By comparison, hepatic pO2 was not reduced significantly in the B. fragilis rats, and pulse rate was similar to controls. Plasma lactate, however, increases more rapidly than in other groups. Survival rates were 100 per cent in the B. fragilis group, 88 per cent in the E. coli group, and 65 per cent in the combined group. The difference between the latter groups was not significant. Hepatic histology was normal in rats of the B. fragilis group at 7 days postchallenge. In survivors of the E. coli and combined inoculum groups, there was evidence of anoxic damage and occasional foci of neutrophilic infiltration. Liver cultures were more often positive in rats of the combined inoculum group (p less than 0.05), most often for E. coli, than in the other groups. In summary, although the acute effects of E. coli were not changed appreciably by combination with B. fragilis, the higher rate of E. coli liver infection in survivors suggests that its viability was enhanced. The role of hepatic hypoxia in this remains unclear. It is feasible that hypoxic foci provided temporary protection for B. fragilis, enabling the organisms to affect favorably the survival of E. coli.
为了测试兼性厌氧菌与厌氧菌之间的协同作用以及肝脏缺氧在其发展过程中可能发挥的作用,对大鼠进行血管内输注10⁸ 大肠杆菌、10⁹ 脆弱拟杆菌或两者的组合。通过选定的6小时测量评估急性效应,包括肝脏pO₂,通过对存活7天的大鼠进行肝脏培养和组织学评估长期效应。在急性期,菌血症组的全身动脉压和pO₂与输注生理盐水的对照组无差异。然而,大肠杆菌组和联合给予两种细菌的大鼠肝脏氧供应显著降低(肝脏平均pO₂ 小于10 mmHg,而对照组为20.8 mmHg)。血浆乳酸和脉搏率也显著增加。相比之下,脆弱拟杆菌组大鼠的肝脏pO₂ 没有显著降低,脉搏率与对照组相似。然而,血浆乳酸比其他组增加得更快。脆弱拟杆菌组的存活率为100%,大肠杆菌组为88%,联合组为65%。后两组之间的差异不显著。在攻击后7天,脆弱拟杆菌组大鼠的肝脏组织学正常。在大肠杆菌组和联合接种组的存活者中,有缺氧损伤的证据和偶尔的中性粒细胞浸润灶。联合接种组大鼠的肝脏培养物阳性率更高(p<0.05),最常见的是大肠杆菌,高于其他组。总之,虽然大肠杆菌与脆弱拟杆菌联合后的急性效应没有明显改变,但存活者中大肠杆菌肝脏感染率较高表明其生存能力增强。肝脏缺氧在其中的作用尚不清楚。缺氧灶为脆弱拟杆菌提供临时保护,使这些微生物能够对大肠杆菌的存活产生有利影响,这是可行的。