["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.", '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).', '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 lymph samples by size, it appears that the putative EC cytotoxic mediator(s) is larger than 100,000 d.'] Are factors larger than 100 kd in post-hemorrhagic shock mesenteric lymph toxic for endothelial cells?