Pronounced reduction of in vivo prostacyclin synthesis in humans by acetaminophen (paracetamol).
The effect of a single dose of 500 mg acetaminophen (paracetamol) on the in vivo synthesis of prostacyclin was studied in healthy volunteers by measurements of the urinary excretion of 2,3-dinor-6-keto-PGF1 alpha. Acetaminophen caused a marked reduction of prostacyclin synthesis for 6-8 hours without any obvious effect on the thromboxane synthesis. Thus, acetaminophen may at least theoretically be disadvantageous for patients suffering from diseases where prostacyclin mediated vascular defence mechanisms are activated, like myocardial infarction, deep vein thrombosis and following surgery.
Grèen
K
K
Department of Clinical Chemistry and Blood Coagulation, Karolinska Hospital, Stockholm, Sweden.
Drvota
V
V
Vesterqvist
O
O
D015121:6-Ketoprostaglandin F1 alpha / Q000031:analogs & derivatives / Q000652:urine; D000082:Acetaminophen / Q000494:pharmacology*; D000328:Adult; D003864:Depression, Chemical; D011464:Epoprostenol / Q000096:biosynthesis*; D006801:Humans; D013929:Thromboxane B2 / Q000031:analogs & derivatives / Q000652:urine; D013997:Time Factors
D000082:Acetaminophen; D013929:Thromboxane B2; D015121:6-Ketoprostaglandin F1 alpha; C028965:2,3-dinor-thromboxane B2; C028290:2,3-dinor-6-ketoprostaglandin F1alpha; D011464:Epoprostenol