Key result
Tissue plasminogen activator restores ~60% of baseline coronary flow in a canine acute thrombosis model.
Why the study?
A stable, low-mortality canine model of acute coronary artery thrombosis incorporating intimal injury and responsive to thrombolytic therapy was needed for evaluating reperfusion strategies.
Does tissue plasminogen activator restore coronary flow in a canine model of acute coronary artery thrombosis?
Does tissue plasminogen activator restore coronary flow in a canine model of acute coronary artery thrombosis?
A newly developed canine model of acute coronary artery thrombosis with intimal injury responds predictably to tissue plasminogen activator, providing a useful tool for investigating reperfusion therapies.
Establishes responsive canine thrombosis model for thrombolysis research; leaves open translation to clinical acute coronary syndromes.
A model of coronary artery thrombosis which: (1) provides a stable thrombus; (2) incorporates intimal injury; (3) has a low mortality rate; (4) responds predictably to thrombolytic therapy, and (5) is technically simple, was developed. Intimal injury was produced proximal to a critical stenosis and followed by the infusion of a blood and thrombin mixture into the injured segment. After thrombus formation flow remained absent in all control animals (n = 7). Microscopy showed intimal injury and coronary thrombosis with platelets adherent to the subendothelium. In animals treated with tissue plasminogen activator (n = 7) flow returned to > 60% of baseline at 20.2 +/- 7.7 min and was cyclical. Mortality and complications were infrequent. This model is useful in investigations of reperfusion therapy.
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Gurbel et al. (2008) studied Acute Coronary Artery Thrombosis (n=14). Tissue plasminogen activator vs. Control was evaluated on Return of coronary flow. Tissue plasminogen activator restored coronary flow to >60% of baseline at 20.2 ± 7.7 minutes in a canine model of acute coronary artery thrombosis, whereas flow remained absent in control animals.
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