Key result
Plasma, serum, and platelet extracts from normal subjects significantly stimulated the dose-dependent production of prostacyclin by cultured endothelial cells.
Normal plasma, serum, and platelet extracts contain factors that stimulate prostacyclin production by endothelial cells, suggesting a regulatory role in vascular homeostasis.
Should not yet change practice; hypothesis-generating for endothelial regulation in vascular homeostasis.
The effect of plasma and serum from normal subjects on the production of prostacyclin by cultured porcine endothelial cells was investigated. 2. Both plasma and serum from all subjects studied significantly stimulated the production of prostacyclin by cultured endothelial cells, measured by the radioimmunoassay of its stable metabolite 6-oxoprostaglandin F1 alpha. 3. Serum caused a consistently greater stimulation than plasma from the same individual. The stimulation was dose-dependent and inhibited by indomethacin. Heparin added to serum also inhibited this response. 4. Extracts from isolated washed platelets were tested for their ability to increase prostacyclin production. Extracts from platelets which had been induced to aggregate and release their granule contents in response to thrombin, caused stimulation. 5. These results indicated the invariable presence in plasma and serum of factors that stimulate the production of prostacyclin by endothelial cells in vitro. At least one of these factors is derived from platelets. These factors may be involved in the regulation of prostacyclin production by the vascular endothelium under normal conditions and in disease states.
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Seid et al. (1983) studied this question. Plasma, serum, and platelet extracts was evaluated on Production of prostacyclin by cultured endothelial cells. Plasma, serum, and platelet extracts from normal subjects significantly stimulated the dose-dependent production of prostacyclin by cultured endothelial cells.
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