{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,28]],"date-time":"2026-03-28T02:44:03Z","timestamp":1774665843004,"version":"3.50.1"},"reference-count":19,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2012,7,19]],"date-time":"2012-07-19T00:00:00Z","timestamp":1342656000000},"content-version":"vor","delay-in-days":7931,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["bpspubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["British J Pharmacology"],"published-print":{"date-parts":[[1990,11]]},"abstract":"<jats:p><jats:list list-type=\"explicit-label\">\n<jats:list-item><jats:p>We have investigated the effect of sodium nitroprusside (NP) and glyceryl trinitrate (GTN) on fibrinolysis in anaesthetized rabbits <jats:italic>ex vivo<\/jats:italic> and <jats:italic>in vitro<\/jats:italic> by measurement of euglobulin clot lysis time (ECLT), plasma levels of tissue plasminogen activator (t\u2010PA) activity, plasma t\u2010PA antigen levels and plasminogen activator inhibitor (PAI\u20101) activity.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p><jats:italic>In vivo<\/jats:italic>, NP (30 \u03bcg kg<jats:sup>\u22121<\/jats:sup>), GTN (30 \u03bcg kg<jats:sup>\u22121<\/jats:sup>) and prostacyclin (3 \u03bcg kg<jats:sup>\u22121<\/jats:sup>) caused similar transient decreases in left ventricular systolic pressure. However, while prostacyclin induced near\u2010maximal inhibition of <jats:italic>ex vivo<\/jats:italic> platelet aggregation, NP or GTN had no effect.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p><jats:italic>Ex vivo<\/jats:italic>, NP caused a significant decrease in ECLT and an increase in plasma t\u2010PA activity.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Intravenous co\u2010administration of t\u2010PA (30 \u03bcg kg<jats:sup>\u22121<\/jats:sup>) with NP caused substantial prolongation of plasma t\u2010PA activity, without affecting t\u2010PA antigen levels.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>In whole blood <jats:italic>in vitro<\/jats:italic>, NP (30 \u03bcg kg<jats:sup>\u22121<\/jats:sup>) prevented the time\u2010dependent increase in PAI\u20101 activity and inhibited inactivation of added t\u2010PA (10 ng ml<jats:sup>\u22121<\/jats:sup>).<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>We propose that NP exhibited fibrinolytic activity through increased t\u2010PA activity as a result of inhibition of PAI\u20101 release from platelets. 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