Feuerstein N, Ramwell P W
Br J Pharmacol. 1981 Jun;73(2):511-6. doi: 10.1111/j.1476-5381.1981.tb10450.x.
1 The release of prostaglandins (PGE2, PGF2 alpha, PGI2) and thromboxane A2 (TxA2) from rat lung exposed to E. coli endotoxin, in vivo or in vitro has been studied. 2 Lung strips of endotoxin-treated rats demonstrated a preferential increase of TxA2 and PGF2 alpha and a decrease in the ratio PGI2/TxA2. 3 These data suggest that changes in the proportions of arachidonic acid metabolites might play a role in the pulmonary pathophysiology during endotoxin shock. 4 Incubation of lung strips with endotoxin in vitro failed to stimulate prostaglandin release; paradoxically, it suppressed both the spontaneous and the ionophore-induced prostaglandin release. 5 These findings suggest that the increase in prostaglandin release by the lung following endotoxin administration in vivo is probably mediated by factor(s) generated in endotoxaemia and is not due to a direct action of endotoxin on the lung tissue.
