Cilostazol suppresses neointimal hyperplasia in canine vein grafts

Fabio A Kudo1, Yuka Kondo, Akihito Muto

  • 1Department of Cardiovascular Surgery, Hokkaido University School of Medicine, Sapporo, Hokkaido, Japan.

Surgery Today
|February 10, 2009
PubMed
Abstract

Insights

Cilostazol effectively reduced intimal hyperplasia in canine vein grafts by inhibiting cell proliferation and promoting apoptosis. This suggests cilostazol is a promising therapeutic agent for preventing graft failure.

Area of Science:

  • Vascular Surgery
  • Pharmacology
  • Cell Biology

Background:

  • Intimal hyperplasia is a major cause of vein graft failure.
  • Understanding the cellular mechanisms of intimal hyperplasia is crucial for developing effective treatments.

Purpose of the Study:

  • To determine if cilostazol, a phosphodiesterase inhibitor, can suppress intimal hyperplasia in canine vein grafts.
  • To investigate the effects of cilostazol on cell proliferation and apoptosis in vein grafts.

Main Methods:

  • Canine carotid artery interposition vein grafts were created in 12 beagle dogs.
  • Dogs received either cilostazol (30 mg/day) or placebo orally twice daily starting 7 days pre-surgery.
  • Grafts were harvested at 1 and 4 weeks for histological analysis.

Main Results:

  • Cilostazol significantly reduced cell proliferation at 1 week post-implantation.
  • Intimal and medial thickness were significantly reduced in the cilostazol group at 4 weeks.
  • Apoptosis was significantly higher in the placebo group compared to the cilostazol group at both time points.

Conclusions:

  • Cilostazol effectively suppressed intimal hyperplasia development in canine autogenous vein grafts.
  • The mechanism involves the modulation of cell proliferation and apoptosis.
  • Cilostazol shows potential as a therapeutic agent to improve vein graft patency.

Related Concept Videos

Peripheral Artery Disease III: Interprofessional Care01:27

Peripheral Artery Disease III: Interprofessional Care

Peripheral Artery Disease (PAD) is characterized by narrowed arteries that diminish blood flow to the extremities. Effective management of PAD requires an interprofessional approach involving various healthcare professionals. The critical aspects of interprofessional care for PAD patients focus on risk factor modification, drug therapy, exercise therapy, nutrition therapy, critical limb ischemia care, and interventional radiology and surgical procedures.The primary treatment goal for PAD...
Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists01:23

Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists

Prostacyclin receptor agonists are a class of therapeutic agents integral to managing pulmonary arterial hypertension (PAH). These drugs operate by mimicking the action of prostaglandin I2, or PGI2, a naturally occurring compound in the body.
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...
Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors01:20

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors

Antiplatelet drugs emerge as frontline defenders against the insidious threat of thromboembolic diseases, where abnormal clots obstruct vital blood vessels. These drugs stand as bulwarks, inhibiting platelet aggregation and clot formation, thereby mitigating the risk of life-threatening conditions like myocardial infarction, coronary artery disease, and thrombotic strokes.
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents01:20

Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents

The gastric mucosa produces prostaglandins E2 (PGE2) and prostacyclin (PGI2), crucial in maintaining gastric health. They exert cytoprotective effects, including increasing bicarbonate secretion, releasing protective mucin, reducing gastric acid output, and preventing harmful vasoconstriction. These effects are mediated through various receptors, such as EP1, EP2, EP3, and EP4.
Non-steroidal anti-inflammatory drugs (NSAIDs) can induce peptic ulcers by inhibiting cyclooxygenase, decreasing...