Factors larger than 100 kd in post-hemorrhagic shock mesenteric lymph are toxic for endothelial cells
Factors larger than 100 kd in post-hemorrhagic shock mesenteric lymph are toxic for endothelial cells
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DOI：
10.1067/msy.2001.111698
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发表时间：
2001-03-01
期刊：
影响因子：
3.8
通讯作者：
Deitch, EA
中科院分区：
文献类型：
--
作者：
Adams, CA;Xu, DZ;Deitch, EA
背景。休克后肠系膜淋巴杀死和损伤内皮细胞（ECs），但其毒性作用的机制和介质尚不清楚。因此，在这些研究中，我们研究和表征了可能参与淋巴对ecs毒性作用的潜在因素。在休克前、休克期间和休克后6小时，每小时收集一次大鼠的淋巴，并以几种方式进行处理——包括去除细胞成分、冷冻加热或按分子量分离——之后测试它们的毒性（乳酸脱氢酶作为细胞损伤的标志，台色蓝作为细胞活力的标志）。对照组由中、休克前淋巴和休克后门静脉血浆组成，无EC毒性。休克后1至3小时收集的淋巴导致90%至95%的ECs死亡，并导致乳酸脱氢酶释放增加8至10倍；然而，这种毒性作用在休克后4小时减弱。内毒素中和和免疫细胞去除不能降低淋巴细胞毒性，但补体失活能降低淋巴细胞毒性。结论：失血性休克后1 - 3小时收集的肠系膜淋巴对ECs有毒性，但这种作用在休克后4- 5小时消失，不依赖于免疫细胞或内毒素的存在，但确实涉及补体和其他假设的大于10万d的介质。
Background. Post-shock mesenteric lymph kills and injures endothelial cells (ECs), but neither the mechanism nor the mediators of lymph's toxic effect are known. Thus, in these studies we investigated and characterized potential factors that may be involved in lymph's toxic effect on ECs.Methods. Lymph was collected hourly from rats before shock, during the shock period and for 6 hours post-shock and processed in several ways-including removal of cellular elements, freezing heating, or separation by molecular weight-after which they were tested for toxicity (lactate dehydrogenase as a marker of cell injury and trypan blue as a marker of cell viability).Results. Controls consisting of medium, pre-shock lymph, and post-shock portal vein plasma had no EC toxicity. Lymph collected 1 to 3 hours post-shock resulted in the death of 90% to 95% of ECs and caused an 8- to 10-fold increase in lactate dehydrogenase release; however, this toxic effect waned by 4 hours post-shock. Endotoxin neutralization and immune cell removal did not decrease lymph cytotoxicity but complement inactivation did. By fractionating the toxic 14 lymph samples by size, it appears that the putative EC cytotoxic mediator(s) is larger than 100,000 d.Conclusions, Mesenteric lymph collected 1 to 3 hours after hemorrhagic shock is toxic to ECs, but this effect is lost by 4- to 5-hours post-shock and is not dependent on the presence of immune cells or endotoxin but does involve complement and other putative mediators of greater than 100, 000 d.