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-PGF1α 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-PGF1α production increased to 1.14±0.86 ng/min initially but declined with time. PGE2 production in response to AA 10 μg/min/ml was steady at around 5 ng/min while PGF2α and TXB2 production were only slightly above the control Perifusion of rabbit washed platelet suspensions at a rate of 3X108 plt/ml/min raised 6KPGF1α production. The production was further increased when platelets were pretreated with 1-benzylimidazole (5 mM), along with a concurrent reduction in TXB2 release. Pre-treatment of platelets with aspirin, on the other hand, abolished the increase in 6KPGF1α production. Our data indicated that the vascular smooth muscle cells can efficiently utilize PGH2 produced by platelets to synthesize PGI2.
|Number of pages||8|
|State||Published - May 15 1986|
Bibliographical noteFunding Information:
The authors wish to thank Dr. Bryan of the Upjohn Company for the generous supply of U63557A and Ms. Yolanda Smith for secretarial assistance. The work is supported by a program project grant from NTH (NS-18494).
- vascular wall
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