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  • Title: Endotoxaemia in rats: role of NO, PAF and TXA2 in pulmonary neutrophil sequestration and hyperlactataemia.
    Author: Olszanecki R, Chłopicki S.
    Journal: J Physiol Pharmacol; 1999 Sep; 50(3):443-54. PubMed ID: 10574473.
    Abstract:
    OBJECTIVE AND DESIGN: The involvement of PAF, TXA2 and NO in LPS-induced pulmonary neutrophil sequestration an hyperlactataemia was studied in conscious rats. As pharmacological tools WEB 2170 (PAF receptor antagonist, 20 mg/kg), camongarel (inhibitor of TXA2 synthase, 30 mg/kg), N(G)-nitro L-arginine methyl ester (L-NAME -- non-selective nitric oxide synthase inhibitor, 30 mg/kg) were used. METHODS: Plasma lactate and NO2-/NO3- levels as well as myeloperoxidase (MPO) activity in lung tissue were measured one and five hours after administration of LPS (4 mg/kg(-1)). RESULTS: LPS induced a twofold increase in plasma lactate levels and nearly 10-fold increase in plasma NO2-/NO3- levels five but not one hour after LPS administration. However, LPS-induced increase in pulmonary MPO activity was seen at both time intervals. Neither WEB 2170 nor camonagrel changed one or five hours responses to LPS (lactate, NO2-/NO3-, MPO). L-NAME potentiated LPS-induced rise in MPO activity in the lung and this potentiation was not affected by WEB 2170 or camonagrel. L-NAME supressed plasma NO2-/NO3- response and substantially potentiated plasma lactate response to LPS and both effects were partially reversed by WEB 2170 or camonagrel. CONCLUSIONS: In summary, we demonstrated that PAF and TXA 2 play a role in overproduction of lactate during endotoxaemia in NO-deficient rats. However, these lipids do not mediate endotoxin-induced sequestration of neutrophils in the lung.
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