VASCULAR-RESPONSES TO MONOENOIC PROSTAGLANDIN PRECURSOR DIHOMO-GAMMA-LINOLENIC ACID IN PERFUSED CANINE LUNG

  • 1 January 1977
    • journal article
    • research article
    • Vol. 201  (2) , 417-420
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 produced pulmonary vasoconstriction when given (50-500 .mu.g/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. PGF1.alpha. was vasopressor in both preparations. The DGLA response at 100 .mu.g/kg in the lung was nearly identical with that of AA 25 .mu.g/kg; DGLA 200 .mu.g/kg = AA 50 .mu.g/kg; DGLA 300 .mu.g/kg = AA 100 .mu.g/kg. The DGLA 100 .mu.g/kg response was nearly equal to that with PGF1.alpha. 1 .mu.g/kg. The equipressor dose ratio, DGLA/AA, varied 2.5-5:1 and DGLA/PGF1.alpha. 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.