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Hyperfibrinogenemia in rats treated with meloxicam.
Mónica Moya1, Vilma Campana, Antonio Gavotto
1From Cátedra de Física Biomédica, Facultad de Ciencias Medicas, Universidad Nacional de Córdoba, Santa Rosa, Argentina.
Japanese Heart Journal
|November 28, 2002
Summary
Meloxicam effectively normalized elevated fibrinogen levels in rats with multiple injuries by inhibiting prostaglandin biosynthesis. However, it did not reverse the associated histopathological aortic lesions.
Area of Science:
- Biomedical Science
- Pharmacology
- Cardiovascular Research
Background:
- Fibrinogen elevation is linked to cardiovascular disease risk.
- Prostaglandin biosynthesis influences fibrinogen secretion.
- Meloxicam inhibits prostaglandin synthesis.
Purpose of the Study:
- To investigate meloxicam's effect on fibrinogen levels.
- To assess meloxicam's impact on thoracic aorta histopathology in a rat model of multiple injuries.
Main Methods:
- Rats underwent weekly laparotomies for 30 days to induce multiple injuries (MI).
- Meloxicam (0.065 mg/kg/day) was administered orally to the MI group post-third laparotomy for 10 days.
- Fibrinogen levels were measured via spectrophotometry; thoracic aorta tissues were examined histopathologically.
Main Results:
- Multiple injuries significantly increased fibrinogen levels compared to controls (336.6±7.5 mg/dL vs. 208.7±6.0 mg/dL).
- Meloxicam treatment normalized fibrinogen levels to control values (198±8.7 mg/dL).
- Histopathological analysis revealed endothelial denudation and intima enlargement in 96% of slices in both MI and meloxicam groups, indicating no lesion regression.
Conclusions:
- Meloxicam effectively reduces hyperfibrinogenemia in a rat model of multiple injuries, likely via selective cyclooxygenase-2 (Cox-2) inhibition.
- Despite normalizing fibrinogen, meloxicam did not lead to regression of induced histopathological lesions in the thoracic aorta.