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Published on: June 29, 2015
Effects of antithrombin III treatment in vascular injury model of mice
Akiko Maeda1, Kunio Ohta1, Kazuhide Ohta1
1Department of Pediatrics, Angiogenesis and Vascular Development, Graduate School of Medical Science, Kanazawa UniversityDepartment of Pediatrics, National Hospital Organization Kanazawa Medical Center, Kanazawa, Japan.
Insights
Antithrombin III (ATIII) significantly reduced thrombus formation and inflammation after arterial injury in mice. This suggests ATIII may be a potential therapeutic agent for preventing complications following angioplasty, without affecting vascular remodeling.
Area of Science:
- Cardiovascular Research
- Vascular Biology
- Interventional Cardiology
Background:
- Balloon angioplasty is used for congenital heart disease stenotic lesions.
- Restenosis and thrombosis are common post-procedure complications.
- Mechanisms underlying these complications remain unclear.
Purpose of the Study:
- To investigate the effects of antithrombin III (ATIII) on inflammation, thrombus formation, and vascular remodeling.
- To assess ATIII's potential in mitigating complications after arterial injury.
Main Methods:
- Guidewire-induced femoral artery injury in mice.
- Administration of ATIII or saline intravenously before injury.
- Evaluation of thrombus formation, inflammatory cell infiltration (CD11b density), and neointimal proliferation at 72 hours and 28 days post-injury.
Main Results:
- Saline-treated vessels showed significant thrombus formation 72 hours post-injury; ATIII-treated vessels did not.
- ATIII treatment markedly reduced inflammatory cell infiltration compared to controls.
- Neointimal proliferation levels were similar in both groups at 28 days.
Conclusions:
- High-dose ATIII reduces mural thrombus formation and inflammatory responses after arterial injury.
- ATIII does not appear to alter the vascular remodeling process.
- ATIII shows potential for managing arterial injury complications.
Background:
Balloon angioplasty has recently been adopted as an acceptable form of treatment for stenotic vessel lesions of congenital heart diseases. However, precise mechanisms of restenosis and thrombosis, which are the most common complications after these procedures, are unknown.
Methods:
We examined the effects of antithrombin III (ATIII) on inflammation, thrombus formation, and remodeling of vascular wall after guidewire-induced injury in the femoral artery of mice. ATIII or saline was administered as a bolus intravenous infusion before injury.
Results:
Seventy-two hours after injury, approximately half of the saline-treated vessels showed macroscopic thrombus formation. In contrast, no thrombi were seen in the arteries pretreated with ATIII. Significantly higher levels of inflammation were induced in the injured vessels than in the sham-operated controls, as determined by CD11b-positive cell density in the adventitial area. ATIII treatment resulted in marked reduction of inflammatory cell infiltration. Twenty-eight days after injury, similar levels of neointimal proliferation were found in the injured arteries in both groups.
Conclusions:
Our results suggested that a high dose of ATIII may influence the sequelae of arterial injury by reducing mural thrombus formation and limiting the inflammatory reaction of the vessel wall without altering the process of vascular remodeling.
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