{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,20]],"date-time":"2026-02-20T08:57:29Z","timestamp":1771577849647,"version":"3.50.1"},"reference-count":31,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2001,12,24]],"date-time":"2001-12-24T00:00:00Z","timestamp":1009152000000},"content-version":"vor","delay-in-days":723,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Acta Anaesthesiol Scand"],"published-print":{"date-parts":[[2000,1]]},"abstract":"<jats:p><jats:bold>Background:<\/jats:bold> Paracetamol is a weak cyclo\u2010oxygenase inhibitor <jats:italic>in vitro<\/jats:italic>. A recent study in children has shown that high doses of paracetamol are effective and safe. We studied the effect of propacetamol on haemostasis in adult volunteers.<\/jats:p><jats:p><jats:bold>Methods:<\/jats:bold> Ten volunteers were investigated in a double\u2010blind, randomized, crossover study. They received propacetamol 60 mg kg<jats:sup>\u22121<\/jats:sup> or ketorolac 0.4 mg kg<jats:sup>\u22121<\/jats:sup> in saline i.v. (30 min) in two different sessions. Platelet function was evaluated before the test infusion (S\u20100), two (S\u20102) and 24 h (S\u201024) after the start of the infusion. Coagulation parameters (PT, APTT, factor V and VII activities) were measured at S\u20100, S\u201024 and 48 h (S\u201048).<\/jats:p><jats:p><jats:bold>Results:<\/jats:bold> One of the volunteers had no secondary platelet aggregation in S\u20100 and was excluded from the final analysis. Two hours (S\u20102) after propacetamol and ketorolac administration the adrenaline (0.9 \u03bcg ml<jats:sup>\u22121<\/jats:sup> and 9.0 \u03bcg ml<jats:sup>\u22121<\/jats:sup>) induced maximal platelet aggregation was decreased compared with S\u20100. At S\u20102 platelet aggregation was inhibited more after ketorolac than after propacetamol. At 24 h after ketorolac, but not after propacetamol, there was still a decrease in the adrenaline\u2010induced maximal platelet aggregation. Propacetamol did not affect adenosine diphosphate (ADP)\u2010induced maximal platelet aggregation, whereas ketorolac decreased 3 and 6 \u03bcM ADP\u2010induced maximal platelet aggregation at S\u20102 and S\u201024. However, 2 h after both ketorolac and propacetamol, thromboxane B<jats:sub>2<\/jats:sub> (TxB<jats:sub>2<\/jats:sub>) concentration decreased in platelet rich plasma after 5 min aggregation induced by 8 \u03bcM ADP. Coagulation was unaffected.<\/jats:p><jats:p><jats:bold>Conclusion:<\/jats:bold> Propacetamol 60 mg kg<jats:sup>\u22121<\/jats:sup> i.v. causes reversible platelet dysfunction demonstrated by a decrease in maximal platelet aggregation and TxB<jats:sub>2<\/jats:sub> concentration. After 0.4 mg kg<jats:sup>\u22121 <\/jats:sup>ketorolac i.v. platelet aggregation and TxB<jats:sub>2<\/jats:sub> formation are inhibited more in comparison with propacetamol, and platelet dysfunction is still seen after 24 h.<\/jats:p>","DOI":"10.1034\/j.1399-6576.2000.440113.x","type":"journal-article","created":{"date-parts":[[2003,3,10]],"date-time":"2003-03-10T09:40:36Z","timestamp":1047289236000},"page":"69-74","source":"Crossref","is-referenced-by-count":63,"title":["Platelet dysfunction after intravenous ketorolac or propacetamol"],"prefix":"10.1111","volume":"44","author":[{"given":"T. T.","family":"Niemi","sequence":"first","affiliation":[]},{"given":"J. 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