Thromboxane and prostacyclin release after endotoxin infusion in the rat.

To determine in the rat whether pulmonary artery hypertension accompanies thromboxane release, we sequentially monitored pulmonary and systemic artery pressures and cardiac output. We measured pulmonary and aortic plasma levels of TxB2 as well as 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) in awake unrestrained adult male Sprague-Dawley rats given a single infusion of endotoxin at the relatively high dose commonly administered to this endotoxin-resistant species. At 40 min after endotoxin infusion, both pulmonary and aortic TxB2 and 6-keto-PGF1 alpha levels increased nine-fold and seven-fold above baseline, respectively. In the pulmonary artery, 40 min after infusion, both mediator levels differed significantly from baseline (p less than 0.05), whereas in the aorta, because of marked variance in the response of different animals, only the 6-keto-PGF1 alpha levels achieved significance (p less than 0.05). These changes were associated with a fall in systemic blood pressure and cardiac output, but no demonstrable rise in pulmonary artery pressure (PAP). Despite ultrastructural evidence of vascular injury, these data indicate that in the rat thromboxane and prostacyclin release following a single infusion of endotoxin is not associated with pulmonary hypertension and that increased prostacyclin production may contribute to systemic hypotension.