Answers are grounded in this paper and cite their sources.
This letter questions the clinical translatability of the timing of endotoxin administration in an experimental model of sepsis after major hepatectomy.
Sir Kwon and Qiu demonstrated protective effects of synthetic inhibitor of neutrophil elastase against endotoxin-induced liver injury following experimental partial hepatectomy. The authors state that intravenous administration of endotoxin 48 h after partial hepatectomy is considered to be a model of sepsis after major hepatectomy, but this model is not applied to human endotoxaemia caused by extended hepatectomy or hepatic failure. It has been assumed that small amounts of endotoxin regularly enter the portal circulation from the gut and almost all are removed efficiently by Kupffer cells. In a human model of acute endotoxaemia evoked by a bolus injection of endotoxin, the endotoxin is rapidly cleared from the circulation within 30 min1. Modest endotoxaemia due to surgical insult is transiently observed during or shortly after operations2. However, severe endotoxaemia associated with irreversible hepatic failure can persist until death. I would like to ask the authors the reason why endotoxin was not administered immediately after partial hepatectomy.
No takes yet. Share an insight, caveat, or question.
Tetsuji Fujita (2007) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: