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• W1033463722 abstract "We determined the vascular and airway effects of PGF2α and its mechanism of action on isolated-perfused lungs of rats were isolated and perfused at 50 ml/kg/min with Krebs-Henseleit bicarbonate buffer solution containing 3% bovine serum albumin. The lungs were ventilated with 21% O2 and 5% CO2 at a tidal volume of 2 ml, frequency of 60 per minute and positive end expiratory pressure of 3 cmH2O. Following injection of 50 μg PGF2α into the afferent pulmonary catheter, there was a marked rise in pulmonary arterial pressure (Ppa) and in resistance to airflow across the lung (RL) and a fall in dynamic lung compliance (Cdyn). Double vascular occlusion technique revealed that 29% of the rise in Ppa was due to an increase in upstream and 71% to downstream resistance. Nω-nitro-L-arginine. 100 μm, a NO synthase inhibitor potentiated the Ppa response two-fold with significant change in airway mechanics. Rat atrial natriuretic factor (r-ANF), 40 μg, quickly reversed the changes in Ppa, RL and Cdyn. Infusion of r-ANF prior to PGF2α attenuated the Ppa response by 38%, RL by 44% and Cdyn by 12%. SQ 29548, a thromboxane receptor blocker and Cl, a protein kinase C (PKC) inhibitor, fully blocked both the vascular and airway responses to PGF2α. PGF2α is a constrictor of pulmonary vessels and airways in rat lungs via thromboxane SQ 29548 receptors, thansduced by intracellular PKC." @default.
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• W1033463722 date "1996-01-31" @default.
• W1033463722 modified "2023-09-27" @default.
• W1033463722 title "PGF2α Causes Bronchoconstriction and Pulmonary Vasoconstriction Via Thromboxane Receptors in Rat Lung" @default.
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• W1033463722 doi "https://doi.org/10.3904/kjim.1996.11.1.74" @default.
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