Prostacyclin and thromboxane A2 release in isolated rat lungs.
The influence of platelets and platelet membranes on the generation of prostacyclin (PGI2) and thromboxane A2 (TXA2) by isolated rat lung and porcine aortic endothelial cell, as measured by RIA of their stable end-products, 6-oxo-PGF1 alpha and TXB2 respectively, was studied. After introduction of either aspirin-treated platelets or membranes from aspirin-treated platelets to the perfusate, a 5-fold increase in the amount of 6-oxo-PGF1 alpha and TXB2 in the perfusate was observed. Treatment of the lung with aspirin produced a 50% reduction in the platelet-stimulated release of PGI2 and TXA2. Treatment of the lung with the phospholipase inhibitor, mepacrine, significantly reduced the platelet-stimulated release of PGI2 and TXA2. Incubation of endothelial cells with untreated platelet membranes did not alter the generation of PGI2. These results suggest that platelet-stimulated release of PGI2 and TXA2 occurs via mechanical stimulation of phospholipase A2, liberating arachidonic acid.