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Kinetics of endotoxin and tumor necrosis factor appearance in portal and systemic circulation after hemorrhagic shock in rats.

机译:大鼠失血性休克后门静脉和全身循环中内毒素和肿瘤坏死因子出现的动力学。

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摘要

OBJECTIVE: This study was performed to investigate gut-derived bacterial translocation and the time course of endotoxin (lipopolysaccharide [LPS]) and tumor necrosis factor (TNF) appearance, both in portal and systemic circulation. SUMMARY BACKGROUND DATA: The significance of intestinal bacteria/endotoxin translocation or TNF formation in the development of systemic sepsis has been disputed. METHODS: A rat model of hemorrhagic shock (30-35 mm Hg for 90 min) and resuscitation was used. RESULTS: Bacterial translocation was histologically observed in the small intestinal wall 30 minutes after resuscitation. A significant increase in LPS concentrations was found in the portal vein (91.7 +/- 30.6 pg/mL) at 90 minutes, which remained steady until 150 minutes after shock. Lipopolysaccharide increased in the systemic circulation, the levels became significant at 120 minutes, and peaked (66.5 +/- 39.2 pg/mL) 150 minutes after shock. Tumor necrosis factor concentrations were found to be significantly elevated in both portal and systemic circulation (75.6 +/- 22.1 vs. 58.4 +/- 14.1 pg/mL) at 90 minutes post-shock. Although there was no further increase in TNF concentration in the portal blood. TNF peaked (83.5 +/- 17.7 pg/mL) in systemic circulation at 120 minutes and still was markedly increased at 150 minutes post-shock. In addition, higher LPS and TNF concentrations in systemic circulation were found in the nonsurvivors than in the surviving animals at the end of resuscitation. CONCLUSIONS: These results suggest that hemorrhagic shock may lead to early bacterial translocation in the intestinal wall and transient access of gut-derived LPS and LPS-induced mediators into the circulation predominantly via the portal circulation.
机译:目的:本研究旨在研究门静脉和全身循环中肠道源性细菌移位以及内毒素(脂多糖[LPS])和肿瘤坏死因子(TNF)出现的时间过程。摘要背景数据:肠道细菌/内毒素易位或TNF形成在系统性败血症发生中的重要性已引起争议。方法:使用大鼠失血性休克模型(30-35 mm Hg持续90分钟)并进行复苏。结果:复苏后30分钟,在小肠壁组织学观察到细菌移位。在90分钟时发现门静脉的LPS浓度显着增加(91.7 +/- 30.6 pg / mL),直至休克后150分钟保持稳定。脂多糖在全身循环中增加,在120分钟时水平显着升高,并在休克后150分钟达到峰值(66.5 +/- 39.2 pg / mL)。发现在休克后90分钟,门脉和全身循环中的肿瘤坏死因子浓度均显着升高(75.6 +/- 22.1 vs. 58.4 +/- 14.1 pg / mL)。尽管门静脉血中TNF浓度没有进一步增加。 TNF在120分钟的全身循环中达到峰值(83.5 +/- 17.7 pg / mL),并且在休克后150分钟仍显着增加。另外,在复苏结束时,非幸存者在全身循环中发现的LPS和TNF浓度高于幸存动物。结论:这些结果表明失血性休克可能导致肠道壁早期细菌移位,肠源性LPS和LPS介导的介体主要通过门脉循环短暂进入循环。

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