Abstract
Prostacyclin (PGI2) is a potent inhibitor of platelet aggregation and a vasodilator that is synthesized from prostaglandin endo-peroxides by vascular endothelial and smooth muscle cells1,2. Its action on platelets is mediated by cyclic AMP3–5. Circulating PGI2 has been detected through its inhibitory effect on the accumulation of platelets on collagen strips superfused with blood from anaesthetized and heparinized cats6 and rabbits7 and this led to the suggestion that PGI2 is released continuously into blood passing through the lungs and functions as a circulating hormone that regulates platelet aggregability6–9. Because of its chemical instability, no more sensitive method of detecting circulating PGI2 has been developed and there is doubt over whether PGI2 is present in more physiological conditions10,11. Although 6-keto-PGF1α, the stable non-enzymatic breakdown product of PGI2, has been assayed in human12,13 and rabbit14,15 plasma, uncertainty over the fraction present as PGI2 in the circulation has limited the value of the results obtained. Finally, it has been suggested that 6-keto-PGE1, a metabolic product of PGI2 or 6-keto-PGF1α that can inhibit platelet aggregation16,17, may also function as a circulating hormone18. To resolve these uncertainties, we have now developed a sensitive bioassay for PGI2-like compounds in blood. The results indicate that fresh arterial blood from physiologically normal rabbits contains insufficient PGI2 or 6-keto-PGE1 to affect platelet function.
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Haslam, R., McClenaghan, M. Measurement of circulating prostacyclin. Nature 292, 364–366 (1981). https://doi.org/10.1038/292364a0
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DOI: https://doi.org/10.1038/292364a0
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