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Research Article Free access | 10.1172/JCI115471

Systemic lysis protects against the effects of platelet activation during coronary thrombolysis.

D J Fitzgerald, M Hanson, and G A FitzGerald

Division of Clinical Pharmacology, Vanderbilt University, Nashville, Tennessee 37232.

Find articles by Fitzgerald, D. in: JCI | PubMed | Google Scholar

Division of Clinical Pharmacology, Vanderbilt University, Nashville, Tennessee 37232.

Find articles by Hanson, M. in: JCI | PubMed | Google Scholar

Division of Clinical Pharmacology, Vanderbilt University, Nashville, Tennessee 37232.

Find articles by FitzGerald, G. in: JCI | PubMed | Google Scholar

Published November 1, 1991 - More info

Published in Volume 88, Issue 5 on November 1, 1991
J Clin Invest. 1991;88(5):1589–1595. https://doi.org/10.1172/JCI115471.
© 1991 The American Society for Clinical Investigation
Published November 1, 1991 - Version history
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Abstract

Systemic lysis may protect against the platelet activation and ongoing thrombosis associated with coronary thrombolysis. To address this hypothesis, we compared urokinase and tissue-type plasminogen activator (t-PA) given intravenously in a chronic, canine model of coronary thrombosis. T-PA 10 micrograms/kg per min induced reperfusion in 55 +/- 7 min but complete reocclusion occurred in 9/10 animals. Reocclusion was prevented by combining t-PA with 7E3, an antibody to the platelet glycoprotein IIb/IIIa which abolished ex vivo platelet aggregation. A similar time to reperfusion was seen with urokinase 750-1,000 U/kg per min. In contrast to t-PA, complete reocclusion occurred in only 1/20 cases (P less than 0.001 vs. t-PA), despite evidence of continued platelet activation in vivo and platelet aggregation ex vivo. Furthermore, this did not reflect a difference in the clearance of the two plasminogen activators. However, plasma fibrinogen was undetectable after urokinase in contrast with t-PA. Furthermore, in animals treated with prourokinase 20 micrograms/kg per min, reocclusion (4/7) correlated with the degree of systemic lysis. To determine whether platelet activation modified the response to urokinase, it was combined with 7E3. 7E3 0.8 mg/kg reduced the time to reperfusion with t-PA (30 +/- 5, n = 6; P = 0.025), but not with urokinase (56 +/- 8 vs. 62 +/- 6, P = ns). Systemic lysis protects against the propensity of continued thrombosis during coronary thrombolysis to delay reperfusion and induce reocclusion. This may modify the requirement for adjunctive antiplatelet therapy.

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