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  • Title: Vascular responses to the monoenoic prostaglandin precursor dihomo-gamma-linolenic acid in the perfused canine lung.
    Author: Wicks TC, Ramwell PW, Rose JC, Kot PA.
    Journal: J Pharmacol Exp Ther; 1977 May; 201(2):417-20. PubMed ID: 859105.
    Abstract:
    Dihomo-gamma-linolenic acid (DGLA; 2 mg/kg i.v.), the monoenoic prostaglandin (PG) precursor was reported earlier to produce systemic hypotension in the intact dog. It is shown here to produce pulmonary vasoconstriction when given (50-500 microng/kg) in the pulmonary artery of the isolated perfused canine lung lobe. This effect is similar to that of arachidonic acid (AA), the bisenoic PG precursor. PGF1alpha was vasopressor in both preparations. The DGLA response at 100 microng/kg in the lung was nearly identical with that of AA25 microng/kg; DGLA 200 microng/kg=AA50 microng/kg;DGLA 300microng/kg=AA 100 microng/kg. The DGLA 100 microng/kg response was nearly equal to that with PGF1alpha 1 microng/kg. The equipressor dose ratio, DGLA/AA, varied 2.5 to f1 and DGLA/PGF1alpha was 100:1. DGLA and AA vascular responses were blocked by indomethacin. Linoleic acid, used as a control fatty acid, had no pulmonary pressor action. When a dextran-based artificial perfusate was used, the vasopressor response to DGLA was essentially unchanged from that in the blood-perfused lobe. The effects of DGLA appear to be due to conversion to vasoactive products in the PG biosynthetic pathway. These products are less potent than those formed in the metabolism of AA.
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