Formation of thrombus and microthrombus during acute coronary artery stenosis in experimental dogs[J]. Chinese Heart Journal, 2011, 23(2): 201-204.
    Citation: Formation of thrombus and microthrombus during acute coronary artery stenosis in experimental dogs[J]. Chinese Heart Journal, 2011, 23(2): 201-204.

    Formation of thrombus and microthrombus during acute coronary artery stenosis in experimental dogs

    • AIM: To explore the relation between acute coronary artery stenosis and thrombus and microthrombus. METHODS: Vasoactive substances including thromboxane B2 (TXB2), 6-keto-prostaglandin F1α, lactic acid (LA), fibrinogen and fibronection in coronary sinus were measured, and thoracotomy and pericardiotomy were performed in 16 dogs. Tailor-made micron constrictor was implanted around the left circumflex branch of the coronary artery (LCX) and the LCX was narrowed quantitatively for 60 min. According to electrocardiogram (ECG), the dogs were divided into ST-segment elevation group and ST-segment descent group and the changes of coronary artery blood flow (CBF) and vasoactive substances in coronary sinus in the same group and between the two groups were compared. Histopathological changes of the coronary artery were observed under light microscope. RESULTS: At 60 min after ischemia, CBF in both group A and group B decreased significantly, but the degree of CBF in group B was more reduced than that in group A. The function of platelet aggregation percentage (%), LA and TXB2 increased, whereas fibrinogen, 6-keto-prostaglandin F1α and fibronection decreased, with no significant difference in all the parameters between group A and group B. Histopathological testing showed vascular endothelium cells injury in the coronary artery, platelet aggregation, mural thrombus and microthrombus in microcirculation. CONCLUSIONS: Both ST-segment elevation and descent in ECG may occur during acute coronary artery stenosis and the occurrence can induce vascular endothelium cell injury and thrombus and microthrombus formation. These changes play an important role in unstable angina pectoris of coronary artery disease.
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