Abstract

Production of eicosanoids by deendothelialized aorta in response to continuous infusions of arachidonic acid and platelet suspensions was determined in a rabbit aorta perfusion model. 6-keto-PGF 1α production was stimulated by AA infusion in a dose-related manner. Infusion of AA at 4 μ/ml/min led to an initial production rate of 0.64±0.29 ng/min which gradually increased to 0.93±0. ll ng/min at the 20th min of infusion. When the concentration of AA infusion was increased to 10 μg/ml/min, 6-keto-PGF 1α production increased to 1.14±0.86 ng/min initially but declined with time. PGE 2 production in response to AA 10 μg/min/ml was steady at around 5 ng/min while PGF 2α and TXB 2 production were only slightly above the control Perifusion of rabbit washed platelet suspensions at a rate of 3X10 8 plt/ml/min raised 6KPGF 1α production. The production was further increased when platelets were pretreated with 1-benzylimidazole (5 mM), along with a concurrent reduction in TXB 2 release. Pre-treatment of platelets with aspirin, on the other hand, abolished the increase in 6KPGF 1α production. Our data indicated that the vascular smooth muscle cells can efficiently utilize PGH 2 produced by platelets to synthesize PGI 2.

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