The involvement of prostaglandins and thromboxanes in the response to pulmonary embolism in anaesthetized rabbits and isolated perfused lungs
Todd, M.H.; Cragg, D.B.; Forrest, J.B.; Ali, M.; McDonald, J.W.
Thrombosis Research 30(1): 81-90
1983
ISSN/ISBN: 0049-3848 PMID: 6687961 Document Number: 210263
Embolization of blood clots produced an increased pulmonary artery pressure in vitro and systemic hypotension in vivo. In control anesthetized animals, systemic blood pressure fell by 44.9 .+-. 28.0 mm Hg following embolization and 40% of the animals died within 5 min of embolization. Plasma concentrations of thromboxane B2 (TXB2) and 6-keto-prostaglandin F1.alpha. (6-keto-PGF1.alpha.) were increased by 0.54 .+-. 0.13 ng/ml and 0.41 .+-. 0.25 ng/ml, respectively. Pretreatment of animals with aspirin (ASA), 5 mg/kg or 250 mg/kg, reduced the hypotensive response and the TXB2 and 6-keto-PGF1.alpha. release. Embolization of isolated lungs perfused with blood-free medium induced an increase in pulmonary artery pressure of 32.7 .+-. 21.0 mm Hg and significantly increased the content of TXB2 and 6-keto-PGF1.alpha. in the perfusate. Pretreatment of lungs with indomethacin, 10 .mu.g/ml, reduced the mean pulmonary pressure response to embolization to 10.6 .+-. 4.9 mm Hg and blocked the appearance of TXB2 in the perfusate. Embolization with an agarose clot induced only a 2.58 .+-. 0.8 mm Hg increase in pressure and no detectable TXB2 release. Apparently, embolization of lungs with a blood clot induces the release of TXB2 and 6-keto-PGF1.alpha. The release of these mediators, the hemodynamic responses and mortality were blocked by ASA pretreatment.