Cardiovascular and platelet responses in the dog to the monoenoic prostaglandin precursor dihomo-gamma-linolenic acid.

The monoenoic prostaglandin precursor, dihomo-gamma-linolenic acid (DGLA), in a single dose intravenously (2.0 mg/kg) in dogs, produced a biphasic alteration in systemic arterial pressure (SAP) with a predominant and marked depressor effect. This SAP response is approximately equidepre-sor to the effect of PGE1 5 mug/kg. DGLA had a positive inotropic effect, causing a greater increase in myocardial contractility than PGE1 in an equidepressor dose. The effect of DGLA on MC was not altered by ganglion blockade or beta-adrenergic blockade. Aspirin blocked the sustained depressor response to DGLA but not an initial drop in SAP and increase of MC of very short duration. Aspirin had no effect on PGE1 or PGF1 alpha responses. DGLA caused no thrombocytopenia, but caused a decrease in sensitivity to platelet aggregation. Control fatty acid injections produced variable effects with no resemblances to DGLA responses. It is concluded that DGLA produces direct depressor and positive inotropic responses as well as responses which may be due to conversion to an endoperoxide formed in the biosynthesis of prostaglandins. In contrast, in equidepressor doses, arachidonic acid (AA), the bisenoic prostaglandin precursor, produces a delayed, single-phase depressor effect which may be due to endoperoxide formation alone. Further, the effect of AA on MC is reflex and is blocked by hexamethonium.