The thrombolytic effect of aspirin in animal model

Soumendra K. Karmohapatra, Nighat N. Kahn, Asru K. Sinha

Research output: Contribution to journalArticlepeer-review

6 Scopus citations


Background: The aspirin induced platelet aggregation has been reported to be mediated through the inhibition of platelet prostaglandin synthesis. This compound has also been recently reported to stimulate nitric oxide synthesis in platelets. Since nitric oxide has been reported to produce fibrinogen/ fibrinolytic effect, investigation was carried out to determine fibrinolytic effect of in vivo exposure of platelets to aspirin in normal volunteers on the fibrinolysis of the clotted platelet-rich plasma in vitro. The thrombolytic effect of aspirin in situ was also carried out by injecting aspirin solution in the mice with ADP induced formed thrombi in the coronary artery. Methods and Results: It was found that the clotted platelet-rich plasma prepared from the volunteers (n = 10, F = 5, M = 5) who ingested 150 mg aspirin, began to undergo spontaneous and progressive fibrinolysis for 200 min at 37°C with the generation of fibrin degradation products in the lysate. No such fibrinolysis could be seen in control experiments. When platelet thrombi were produced in the coronary artery of mice by injecting ADP, and these animals subsequently received intravenous injection of aspirin (4 μM final), they not only survived (P < 0.0001, n = 10) the thrombogenic assault but the lysis of the platelet thrombi was also noted in the post mortem examination. The thrombolytic effect of aspirin was found to be comparable to that of streptokinase in these animals. Conclusions Aspirin, through the stimulation of NO synthesis, may produce thrombolysis in vivo.

Original languageEnglish
Pages (from-to)123-129
Number of pages7
JournalJournal of Thrombosis and Thrombolysis
Issue number2
StatePublished - Oct 2007


  • Acute ischemic heart disease
  • Aspirin
  • Nitric oxide
  • Streptokinase
  • Thrombolysis


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