Abstract
Tissue plasminogen activator (t-PA) is a marker of endothelial cell injury or activation. The release of t-PA from isolated rat hearts (Langendorff model) subjected to ischemia-reperfusion or reactive oxygen intermediates (ROI) generated by H 2O 2 was investigated. H 2O 2 (200 μM) increased t-PA activity in the coronary effluent to 305±84% of initial value (mean±SEM, p<0.04 vs controls) at the end of a 10 min intervention. The hydroxyl radical scavenger thiourea (10 mM) only partially inhibited the increase (175±27%, p<0.01 compared to controls). 20 min normothermic ischemia increased t-PA activity to 416±108% (p<0.005 compared to controls) at the start of reperfusion. In conclusion, cardiac injury by ischemia-reperfusion or ROI increases release of t-PA.
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