Journals / Türk Göğüs Kalp Damar Cerrahisi Dergisi / 2012 / Cilt: 20 - Sayı: 3

Klopidogrel, asetilsalisilik asit ve tirofibanın sıçan torasik aort segmentlerinde asetilkolin ile uyarılan gevşeme üzerine etkisi

The effects of clopidogrel, acetyl salicylic acid and tirofiban on acetylcholine-induced dilation in rat thoracic aorta segments

Pages
584–589
Publication Date
2022-09-02
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

These findings suggest that ASA and clopidogrel may have a limited effect on endothelium-mediated vasodilation.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Background: In this article, we aimed to investigate the effects of antithrombotic agents, including acetyl salicylic acid (ASA), clopidogrel, and tirofiban on the acetylcholine (ACh)- induced dilation responses in rat thoracic aorta segments.
📊
Key Findings & Data:Methods: Twenty-eight Wistar albino male rats weighing between 250-300 g were included in the study.
💡
Conclusion & Impact:These findings suggest that ASA and clopidogrel may have a limited effect on endothelium-mediated vasodilation.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

Background: In this article, we aimed to investigate the effects of antithrombotic agents, including acetyl salicylic acid (ASA), clopidogrel, and tirofiban on the acetylcholine (ACh)- induced dilation responses in rat thoracic aorta segments. Methods: Twenty-eight Wistar albino male rats weighing between 250-300 g were included in the study. The rats were randomly divided into four groups: the ASA group (n=7), the clopidogrel group (n=7), the tirofiban group (n=7), and the control group (n=7). Intraperitoneal (IP) injection of ASA (1.5 mg/kg) or clopidogrel (1 mg/kg) was administered 12 hours before the experiment. In the tirofiban group, 150 μgr/kg tirofiban IP was given twice at one and 12 hours before the experiment. The rats in the control group did not receive any medication. After the rats were decapitated, the segments of the thoracic aorta were removed and suspended in an oxygenated Krebs solution in a tissue bath, and the dose dependency in the responses to the ACh-induced dilation in the aortic rings were studied. Results: The dilation responses of the aortic rings to ACh in the lowest molar concentration (10-9) were found to be reduced in the ASA (94.3%±3.3) and clopidogrel (94.6%±3.1) groups when compared with the control group (86.7%±8.1) (p<0.05). The responses to higher concentrations of ACh were observed to be similar in all of the groups. Conclusion: Acetyl salicylic acid and clopidogrel treatments resulted in a slight delay of endotheliummediated relaxation while tirofiban had no significant effect. These findings suggest that ASA and clopidogrel may have a limited effect on endothelium-mediated vasodilation.

Özet

Amaç: Bu çalışmada, asetilsalisilik asit (ASA), klopidogrel ve tirofiban gibi antitrombositer ajanların sıçan torasik aort segmentinde asetilkolin (ACh) ile uyarılan gevşeme yanıtları üzerine olan etkileri araştırıldı. Çalışma planı: Yirmi sekiz adet ağırlıkları 250-300 g arasında olan Wistar-albino türü yetişkin erkek sıçan çalışmaya alındı. Sıçanlar randomize olarak dört gruba ayrıldı: ASA grubu (n=7), klopidogrel grubu (n=7), tirofiban grubu (n=7) ve kontrol grubu (n=7). Deneyden 12 saat önce intraperitoneal (İP) ASA (1.5 mg/kg) veya klopidogrel (1 mg/kg) enjeksiyonları yapıldı. Tirofiban grubunda, 150 μgr/kg tirofiban İP deneyden 1 ve 12 saat önce olmak üzere, iki kez verildi. Kontrol grubundaki sıçanlara herhangi bir ilaç verilmedi. Sıçanlar dekapite edildikten sonra torasik aort segmentleri çıkartıldı ve oksijenize Krebs çözeltisi içinde organ banyosuna asıldı ve aort halkalarında asetilkolin ile uyarılan gevşeme yanıtının doza bağımlı değişimleri incelendi. Bulgular: Asetilkolinin en düşük molar konsantrasyonu (10-9) ile elde edilen gevşeme yanıtının ASA (%94.3±3.3) ve klopidogrel (%94.6±3.1) grubunda kontrol (%86.7±8.1) grubuna göre azalmış olduğu bulundu (p<0.05). Daha yüksek asetilkolin konsantrasyonlarında ise, tüm gruplarda gevşeme yanıtlarının benzer olduğu gözlemlendi. Sonuç: Asetilsalisilik asit ve klopidogrel tedavilerinin sonucunda endotel aracılı gevşeme yanıtında hafif bir gecikme ortaya çıkmış ve tirofibanın belirgin bir etkisi olmamıştır. Bu bulgular ASA ve klopidogrelin endotel aracılı vazodilatasyon üzerinde sınırlı bir etkisi olabileceğini düşündürmektedir.

🔖

Cite This Article

BOĞA, M., ÖZKISACIK, E. A., KURTOĞLU, T., GÜRCÜN, U., DURMAZ, S., DİŞCİGİL, B., BADAK, M. İ. (2022). Klopidogrel, asetilsalisilik asit ve tirofibanın sıçan torasik aort segmentlerinde asetilkolin ile uyarılan gevşeme üzerine etkisi. Türk Göğüs Kalp Damar Cerrahisi Dergisi, Cilt: 20 - Sayı: 3, 584–589. https://ajindex.com/articles/424745

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (12)

  1. Braunwald E, Antman EM, Beasley JW, Califf RM, Cheitlin MD, Hochman JS, et al. ACC/AHA guideline update for the management of patients with unstable angina and non-STsegment elevation myocardial infarction-2002: summary article: a report of the American College of Cardiology/ American Heart Association Task Force on Practice Guidelines (Committee on the Management of Patients With Unstable Angina). Circulation 2002;106:1893-900
  2. Antman EM, Anbe DT, Armstrong PW, Bates ER, Green LA, Hand M, et al. ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarctionexecutive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1999 Guidelines for the Management of Patients With Acute Myocardial Infarction). Circulation 2004;110:588-636
  3. Norgren L, Hiatt WR, Dormandy JA, Nehler MR, Harris KA, Fowkes FG,et al. Inter-Society Consensus for the Management of Peripheral Arterial Disease (TASC II). J Vasc Surg 2007;45 Suppl S:S5-67
  4. Chaturvedi S, Bhattacharya P. New insights in antiplatelet therapy for patients with ischemic stroke. Neurologist 2011;17:255-62
  5. Ueno M, Kodali M, Tello-Montoliu A, Angiolillo DJ. Role of platelets and antiplatelet therapy in cardiovascular disease. J Atheroscler Thromb 2011;18:431-42
  6. Vane JR, Anggård EE, Botting RM. Regulatory functions of the vascular endothelium. N Engl J Med 1990;323:27-36
  7. Jaffe EA. Cell biology of endothelial cells. Hum Pathol 1987;18:234-9
  8. Discigil B, Evora PR, Pearson PJ, Viaro F, Rodrigues AJ, Schaff HV. Ionic radiocontrast inhibits endotheliumdependent vasodilation of the canine renal artery in vitro: possible mechanism of renal failure following contrast medium infusion. Braz J Med Biol Res 2004;37:259-65
  9. Evora PR, Pearson PJ, Discigil B, Oeltjen MR, Schaff HV. Pharmacological studies on internal mammary artery bypass grafts. Action of endogenous and exogenous vasodilators and vasoconstrictors. J Cardiovasc Surg (Torino) 2002;43:761-71
  10. Evora PR, Pearson PJ, Chua YL, Discigil B, Schaff HV. Exogenous hyaluronidase induces release of nitric oxide from the coronary endothelium. J Thorac Cardiovasc Surg 2000;120:707-11
  11. Lee TK, Chen YC, Lien IN, Liu MC, Huang ZS. Inhibitory effect of acetylsalicylic acid on platelet function in patients with completed stroke or reversible ischemic neurologic deficit. Stroke 1988;19:566-70
  12. Yasuda O, Takemura Y, Kawamoto H