[Increase of pulmonary vascular resistance and permeability due to the metabolism of free arachidonic acid (author's transl)].
Release and metabolism of arachidonic acid are supposed to form the common final pathway of different stimuli on the pulmonary vascular endothelium. In a model of isolated, ventilated and perfused rabbit lungs we investigated the influence of increased availability of free arachidonic acid on pulmonary vascular resistance and permeability. Addition of arachidonic acid to the perfusion fluid or release of arachidonic acid by Ca-ionophore A 23187 regularly produces a characteristic biphasic increase of the pulmonary vascular resistance as well as a continuous increase in permeability, followed by pulmonary edema. Inhibition of cyclooxygenase by indomethacin prevents the augmentation of vascular resistance, the increase of vascular permeability however is enhanced. thus the raise in pulmonary vascular resistance can be ascribed to cyclooxygenase products, the increased pulmonary vascular permeability to lipoxygenase products of arachidonic acid.
D000818:Animals; D001095:Arachidonic Acids / Q000378:metabolism*; D001241:Aspirin / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects; D002199:Capillary Permeability / Q000187:drug effects; D005260:Female; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D011652:Pulmonary Circulation / Q000187:drug effects; D011817:Rabbits; D014655:Vascular Resistance / Q000187:drug effects
D001095:Arachidonic Acids; D001241:Aspirin; D007213:Indomethacin
Zunahme des Strömungswiderstandes und der Gefässpermeabilität in der pulmonalen Strombahn als Folge des Metabolismus freier Arachidonsäure.