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Effects of Ticlopidine on Platelet Aggregation in Beagles with Unstable Angina

Received: 12 February 2017    Accepted: 4 March 2017    Published: 21 March 2017
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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-1 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-1 administration. CFRs were abolished and did not return when AD was infused after TC 32 mg•kg-1 administration. (2)The time for CFRs absolute disappearance of TC in dose of 32 mg•kg-1 was shorter than that in control group. (3)The platelet aggregation induced by ADP was inhibited obviously after TC 16,32 mg•kg-1 administration, and the aggregation in TC 32 mg•kg-1 didn’t return after AD administration. Conclusion TC had dose-dependent antiplatelet effects in beagles, suggesting TC has reliable therapeutical efficacy on angina pectoris.

Published in Science Journal of Clinical Medicine (Volume 6, Issue 1)
DOI 10.11648/j.sjcm.20170601.12
Page(s) 20-23
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This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2024. Published by Science Publishing Group

Keywords

Ticlopidine, Antiplatelet Aggregation, Unstable Angina Pectoris

References
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[2] Dasbiswas A, Rao MS, Babu PR, Vijayvergiya R, Nayak R, Dani S, et al. A comparative evaluation of prasugrel and clopidogrel in patients with acute coronary syndrome undergoing percutaneous coronary intervention. J Assoc Physicians India. 2013, 61 (2): 114-116, 126.
[3] Folts JD, Stamler J, Loscalzo J. Intravenous nitroglycerin infusion inhibits cyclic blood flow responses caused by periodic platelet thrombus formation in stenosed canine coronary arteries. Circulation 1991; 83 (6): 2122-7.
[4] Wang Wei-Ting, Zhao Zhuan-You, Liu Hou-Xiao. The Establishment of the Model of Unstable Angina Pectoris and the Evaluation of Heparin Sodium. Journal of China Pharmaceutical University 2002; 33 (supl): 172-175.
[5] Osman HE. Grape juice but not orange or grapefruit juice inhibits platelet activity in dogs and monkeys (macaca fasciularis). J Nutr 1998, 128: 2307-2312.
[6] Maalej, N. Hoden, JE. Folts, JD. Effect of Shear Stress on Acute Platelet Thrombus Formation in Canine Stenosed Carotid Arteries: An In Vivo Quantitative Study. J Throm Thrombolysis 1998, 5 (3): 231-238.
[7] Folts JD, Rowe GG. Epinephrine potentiation of in vivo stimuli reverses aspirin inhibition of platelet thrombus formation in stenosed canine coronary arteries. 1988; 50 (4): 507-16.
[8] Davi, G. and Patrono, C. Platelet Activation and Atherothrombosis. New England Journal of Medicine, 2007, 357 (24), 2482-2494
[9] Becker R C. Platelet Biology: The Role of Platelets in Hemostasis, Thrombosis and Inflammation [J]. American Journal of Cardiology, 2014, 83 (9A): 3E-6E.
[10] Shaker A. Mousa; Ram Kapil; Dun-Xu Mu. Intravenous and Oral Antithrombotic Efficacy of the Novel Platelet GPIIb/IIIa Antagonist Roxifiban (DMP754) and Its Free Acid Form, XV459 Arteriosclerosis, Thrombosis, and Vascular Biology 1999; 19: 2535-2541.
[11] Ikeda H, Koga Y, Kuwano K, Nakayama H, Ueno T, Yoshida N, et al. Cyclic flow variations in conscious dog model of coronary artery stenosis and endothelial injury correlate with acute ischemic heart disease syndromes in humans. J Am Coll Cardiol 1993; 21 (4): 1008-1017.
[12] Zhang S, Sun C, Hu H, He Y, Yao Y, Cao Y, Zeng Z. Effects of Paclitaxel on the Ability of Aspirin and Clopidogrel to Inhibit Platelet Aggregation. Clin Appl Thromb Hemost. 2016, 22 (7): 673-678.
[13] Christ G, Hafner T, Siller-Matula J M, et al. Platelet Inhibition by Abciximab Bolus-Only Administration and Oral ADP Receptor Antagonist Loading in Acute Coronary Syndrome Patients: The Blocking and Bridging Strategy. Thrombosis research, 2013, 132 (1): e36.
[14] Weisman G A, Woods L T, Erb L, et al. P2Y receptors in the mammalian nervous system: pharmacology, ligands and therapeutic potential.[J]. CNS & neurological disorders drug targets, 2012, 11 (6): 722-38.
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    Weiting Wang, Chunhua Hao, Zhuanyou Zhao. (2017). Effects of Ticlopidine on Platelet Aggregation in Beagles with Unstable Angina. Science Journal of Clinical Medicine, 6(1), 20-23. https://doi.org/10.11648/j.sjcm.20170601.12

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    ACS Style

    Weiting Wang; Chunhua Hao; Zhuanyou Zhao. Effects of Ticlopidine on Platelet Aggregation in Beagles with Unstable Angina. Sci. J. Clin. Med. 2017, 6(1), 20-23. doi: 10.11648/j.sjcm.20170601.12

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    AMA Style

    Weiting Wang, Chunhua Hao, Zhuanyou Zhao. Effects of Ticlopidine on Platelet Aggregation in Beagles with Unstable Angina. Sci J Clin Med. 2017;6(1):20-23. doi: 10.11648/j.sjcm.20170601.12

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  • @article{10.11648/j.sjcm.20170601.12,
      author = {Weiting Wang and Chunhua Hao and Zhuanyou Zhao},
      title = {Effects of Ticlopidine on Platelet Aggregation in Beagles with Unstable Angina},
      journal = {Science Journal of Clinical Medicine},
      volume = {6},
      number = {1},
      pages = {20-23},
      doi = {10.11648/j.sjcm.20170601.12},
      url = {https://doi.org/10.11648/j.sjcm.20170601.12},
      eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.sjcm.20170601.12},
      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-1 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-1 administration. CFRs were abolished and did not return when AD was infused after TC 32 mg•kg-1 administration. (2)The time for CFRs absolute disappearance of TC in dose of 32 mg•kg-1 was shorter than that in control group. (3)The platelet aggregation induced by ADP was inhibited obviously after TC 16,32 mg•kg-1 administration, and the aggregation in TC 32 mg•kg-1 didn’t return after AD administration. Conclusion TC had dose-dependent antiplatelet effects in beagles, suggesting TC has reliable therapeutical efficacy on angina pectoris.},
     year = {2017}
    }
    

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  • TY  - JOUR
    T1  - Effects of Ticlopidine on Platelet Aggregation in Beagles with Unstable Angina
    AU  - Weiting Wang
    AU  - Chunhua Hao
    AU  - Zhuanyou Zhao
    Y1  - 2017/03/21
    PY  - 2017
    N1  - https://doi.org/10.11648/j.sjcm.20170601.12
    DO  - 10.11648/j.sjcm.20170601.12
    T2  - Science Journal of Clinical Medicine
    JF  - Science Journal of Clinical Medicine
    JO  - Science Journal of Clinical Medicine
    SP  - 20
    EP  - 23
    PB  - Science Publishing Group
    SN  - 2327-2732
    UR  - https://doi.org/10.11648/j.sjcm.20170601.12
    AB  - 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-1 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-1 administration. CFRs were abolished and did not return when AD was infused after TC 32 mg•kg-1 administration. (2)The time for CFRs absolute disappearance of TC in dose of 32 mg•kg-1 was shorter than that in control group. (3)The platelet aggregation induced by ADP was inhibited obviously after TC 16,32 mg•kg-1 administration, and the aggregation in TC 32 mg•kg-1 didn’t return after AD administration. Conclusion TC had dose-dependent antiplatelet effects in beagles, suggesting TC has reliable therapeutical efficacy on angina pectoris.
    VL  - 6
    IS  - 1
    ER  - 

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Author Information
  • State Key Laboratory of Pharmacokinetics and Pharmacodynamics, Tianjin Institute of Pharmaceutical Research, Tianjin, China

  • State Key Laboratory of Pharmacokinetics and Pharmacodynamics, Tianjin Institute of Pharmaceutical Research, Tianjin, China

  • State Key Laboratory of Pharmacokinetics and Pharmacodynamics, Tianjin Institute of Pharmaceutical Research, Tianjin, China

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