Abstract
Aim To study the antiplatelet aggregation of ticlopidine (TC). Methods Using coronary artery Folts, model in beagles, the efficacy of TC on platelet aggregation was studied. Results (1)TC16, 32 mg•kg<sup>-1</sup> dramatically inhibited the frequency of CFRs dose-dependently, and the times of CFRs decreased by 27%, 56%, 95%, 100% respectively at 1-4 h than that in control group’s after TC 32 mg•kg<sup>-1</sup> administration. CFRs were abolished and did not return when AD was infused after TC 32 mg•kg<sup>-1</sup> administration. (2)The time for CFRs absolute disappearance of TC in dose of 32 mg•kg<sup>-1</sup> was shorter than that in control group. (3)The platelet aggregation induced by ADP was inhibited obviously after TC 16,32 mg•kg<sup>-1</sup> administration, and the aggregation in TC 32 mg•kg<sup>-1</sup> didn’t return after AD administration. Conclusion TC had dose-dependent antiplatelet effects in beagles, suggesting TC has reliable therapeutical efficacy on angina pectoris.
Highlights
It was extensively applied in unstable angina pectoris (UAP), acute myocardial infarction (AMI), transient ischemic attack (TIA), stroke in clinics [1, 2], but still no experimental studies showed that it was effective in models of UAP
TC 16, 32 mgkg-1 dramatically inhibited the frequency of cycle flow reductions (CFRs) dose-dependently, and the frequency of CFRs decreased by 87%, 100% respectively at 1-4 h than that in control group’s
The unstable angina pectoris was mostly related to cracking of atherosclerosis clotty [9], and platelet aggregation and releasing were important in coronary arterial thrombus formation [10]
Summary
More and more evidence demonstrated that platelet plays an important role in atherosclerosis, and arterial thrombus formation. Antiplatelet treatment became one of the most important techniques for cardio- and cerebro- vascular disease. Unlike aspirin (ASA), Ticlopidinee (TC) was an inhibitor of platelet aggregation acted on some agonists such as ADP, adrenalin (AD), arachidonic acid (AA), thrombin (Th), collagen (CG), 5-HT et al, especifically inhibited ADP-induced platelet aggregation without affecting prostaglandin metabolism. It was extensively applied in unstable angina pectoris (UAP), acute myocardial infarction (AMI), transient ischemic attack (TIA), stroke in clinics [1, 2], but still no experimental studies showed that it was effective in models of UAP.
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