Abstract
A new rabbit lung-heart preparation has been developed in order to evaluate the heart effects of the unstable PG’s (PGI2, TXA2) released by the lungs. The lungs were perfused (30 ml/min) and the effluent was used by the heart for anterograd constant pressure coronary perfusion. The coronary flow and the pulmonal perfusion pressure were recorded. Injections of arachidonic acid (AA, 10-100 μg) and the Ca+ +-ionophore A-23187 (50 μg) into the lungs caused a rapid increase in perfusion pressure and an increase in coronary flow. The first effect was inhibited by indomethacin (Indo) and N-butylimidazole (NBI, a TXA2-inhibitor), while the second effect was blocked only by Indo. The increase in coronary flow was not affected by selective administration of Indo through the left atrium. This effect was probably due to PGI2-release from the lungs. Embolization with 20-50 mg Sephadex S-25 microspheres caused an increase in the perfusion pressure, which was inhibited by Indo and NBI. Repeated injections of AA and A-23187 after embolization caused a paradoxical decrease in coronary flow, and this was blocked by both inhibitors. This may reflect a shift of AA metabolism from PGI2 to TXA2.
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