Abstract
Hepatic metabolism of prostacyclin (PGI2) results in the formation of several biologically inactive lipids and one stable product that has the same chromatographic and biological properties as authentic 6-keto PGE1. Both prostaglandins, 6-keto PGE1 and PGI2, have comparable potency in their antiaggregatory and disaggregatory effects on platelets. They contract the superfused rat stomach strip but differ in their effects on the bovine coronary artery, which is contracted by 6-keto PGE1 but relaxed by PGI2. Further, 6-keto PGE1 is considerably more stable than PGI2. Thus, 6-keto PGE1 could account for some of the prolonged effects occasionally seen with PGI2.
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