PubMed · 1510815
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J A Majde. 1992. Endotoxin detection.. https://doi.org/10.1016/0167-5699(92)90047-b
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The treatment of septic shock remains a major problem in surgical practice. Current research on the pathogenesis of the sepsis syndrome focuses on the effects of the lipopolysaccharide constituents of bacterial endotoxin. Evidence suggests that endotoxin induces a whole-body inflammatory response that in turn mediates organ damage, eventually leading to multiorgan failure. The first organ in which failure is usually apparent is the lung, with the appearance of non-cardiogenic pulmonary oedema as part of the adult respiratory distress syndrome. Inflammatory cells involved in lung injury include neutrophils and macrophages, which release mediators such as elastase, oxygen radicals and cytokines. This review summarizes current experimental work on how endotoxin leads to lung injury, based on its effects in animals and patients. Present knowledge suggests that future treatment of septic shock might involve inhibiting the body's inflammatory response to endotoxin. Possible ways of doing this are discussed.
Phospholipase A2 (PLA2) activity was measured in the serum of 23 individuals infused intravenously with endotoxin (EN) at a dose of 4 ng/kg body weight. A marked increase in PLA2 was noted 3 h after EN challenge (mean 828 +/- 513 units/ml), reached its maximum at 24 h after the challenge (mean 2667 +/- 2442 units/ml), and was still evident at 48 h (mean 763 +/- 366 units/ml). In contrast, TNF levels were maximal (mean 712 +/- 375 pg/ml) 90 min after the EN challenge and subsided to very low values (5 +/- 5 pg/ml) 5 h after the challenge. There was a positive correlation between the maximum response of TNF and that of PLA2 (r = 0.82, P < 0.01). Administration of ibuprofen or pentoxifylline did not alter the PLA2 response. EN challenge did not affect serum pancreatic PLA2 concentration or that of the lysosomal cationic enzyme, lysozyme. Neutralizing antibody against human recombinant (synovial type) PLA2 completely abolished PLA2 activity in the sera tested. We conclude that EN infusions cause marked intravascular release of nonpancreatic secretory PLA2 and that the magnitude of this response seems to be related to the prior generation of TNF.