Increased prostaglandin I 2 and thromboxane A 2 production by rat dental pulp after intravenous administration of endotoxin

Abstract

The effect of systemic endotoxin (lipopolysaccharide from Escherichia coli 0111:B4) on prostaglandin I 2 (PGI 2) and thromboxane A 2 (TXA 2) production by rat dental pulp was investigated. Intravenous injection of endotoxin increased ex vivo production of both PGI 2 and TXA 2 by the pulp tissue, when determined by radioimmunossay. A significant effect on PGI 2 and TXA 2 production was observed with endotoxin doses of greater than 2 and 0.4 mg/kg, respectively. A significant increase was also observed at 30 min after injection of 10 mg/kg endotoxin, reaching a maximum after 60 min for both PG and TX production. Endotoxin (10 mg/kg for 60 min) also increased TXA 2 but not PGI 2 production in lung tissue, but had no effect in jejunal tissue. Indomethacin (10 μM) completely inhibited PGI 2 and TXA 2 production by the pulp of physiological saline- and endotoxin-treated rats. Further, arachidonic acids (10 μM) significantly increased PG and TX production by the pulp of saline- but not of endotoxin-treated rats. Endotoxin (100 μg/ml) had no in vitro effect on PG or TX production when incubated with isolated pulp, lung and jejunal tissues, suggesting that the endotoxin-induced increases in PG and TX production are an indirect effect. The endotoxin-induced increase in TXA 2 production, but not in PGI 2 production, by the pulp tissue was significantly suppressed by WEB 2170, a platelet-activating factor (PAF) antagonist. These results indicate that arachidonate metabolism in pulp tissue is susceptible to endotoxaemia in comparison with the lung and jejunum, and further suggest that the endotoxin-induced increase in, at least, TXA 2 production by the pulp is mediated by PAF.