Why the study?
Do pharmacological interventions (thromboxane synthetase inhibitor, heparin, argatroban, urokinase) prevent acute myocardial infarction in a canine model of acute coronary syndromes?
Do pharmacological interventions (thromboxane synthetase inhibitor, heparin, argatroban, urokinase) prevent acute myocardial infarction in a canine model of acute coronary syndromes?
In a canine model of acute coronary syndromes, intravenous administration of argatroban, heparin, or a thromboxane synthetase inhibitor significantly reduced the incidence of acute myocardial infarction.
Hypothesis-generating for antithrombotic prevention of AMI in experimental ACS; leaves open translation to human therapy.
Intracoronary thrombodynamics in acute coronary syndromes was studied with an experimental canine model. An intracoronary thrombus was precipitated at the mock ruptured atheromatous plaque consisting of cholesterol and collagen. In 8 of 10 control models, acute myocardial infarction (AMI) was induced by intracoronary occlusive thrombus 1 h after the start of the experiment. Coronary blood flow decreased continuously (Type A, n = 5) or cyclically (Type B, n = 3) to end in AMI. Effects of pharmacological interventions to prevent AMI were also studied with the model. An intravenous bolus injection of a thromboxane synthetase inhibitor (RS-5186), heparin, a thrombin inhibitor (argatroban), and a thrombolytic agent (urokinase) was performed in 10 models for each drug. The incidence of AMI was significantly decreased to 3 of the 10 models injected with the thromboxane synthetase inhibitor and heparin (p < .05, each drug group vs. control). The preventive effect of argatroban was more potent and AMI occurred in 2 of 10 models (p < 0.01, argatroban vs control).
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Haruo Tomoda (1992) studied this question.
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