Prostacyclin is required for t-PA release after venous occlusion

L. Iacoviello, A. De Curtis, M. C. D'Adamo, C. Amore, W. Buczko, G. De Gaetano, M. B. Donati

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The role of vascular cyclooxygenase pathway on tissue-type plasminogen activator (t-PA) release after venous occlusion was studied in anesthetized rats. After the inferior vena cava was clamped for 30 min, fibrinolytic activity increased from 143.7 ± 14.5 to 209.5 ± 10.3 mm2 (means ± SE, P <0.002). This increase was prevented by aspirin at high (100 mg/kg iv) but not at low doses (1 mg/kg iv). Dazoxiben (10 mg/kg iv), an inhibitor of thromboxane synthase, was ineffective on the fibrinolytic response. Both the basal levels of 6-ketoprostaglandin F(1α) and its increase after venous occlusion were suppressed by 100 mg/kg aspirin administration (from 0.64 ± 0.2 to 0.05 ± 0.002 ng/ml before occlusion, P <0.001; and from 1.08 ± 0.2 to 0.06 ± 0.002 ng/kg after occlusion, P <0.001), whereas they were both unaffected by aspirin at low doses (from 0.53 ± 0.06 before to 1.20 ± 0.08 ng/ml after stasis). Moreover, iloprost, a stable analogue of prostacyclin, reversed the aspirin inhibitory effects on fibrinolytic activity by restoring t-PA vascular release after venous stasis. Our results provide experimental evidence that an intact cyclooxygenase pathway in vascular wall is required for the fibrinolytic activity increase after venous occlusion in rats.

Original languageEnglish
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number2 35-2
Publication statusPublished - 1994


  • aspirin
  • cyclooxygenase
  • rats
  • vascular endothelium

ASJC Scopus subject areas

  • Physiology
  • Agricultural and Biological Sciences(all)


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