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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.
Abstract:
Fibrinogen secretion is mediated by prostaglandin biosynthesis and is considered a risk factor for cardiovascular disease. Since meloxicam produces inhibition of prostaglandin biosynthesis it may help to normalize hyperfibrinogenemia. We investigated the pharmacological effect of meloxicam on fibrinogen levels and the possible regression of histopathological lesions of thoracic aorta. Rats were subjected to multiple injuries (MI) in the form of laparotomies (Lx) during a 30 day period (1/week). Meloxicam 0.065 mg/kg/day (per rat) was administered orally immediately after the third Lx in multiple injury animals during a ten day period. Blood was obtained 72 hours after the last injury in all groups. Fibrinogen was measured by spectrophotometry and the values were expressed in mg/dL. A statistically significant increment of fibrinogen was observed when comparing uninjured animals (control) (208.7+/-6.0) with the multiple injury group (336.6+/-7.5) (P<0.001). Fibrinogen decreased to the control value in the meloxicam group (198+/-8.7). Histopathological lesions were similar in the MI and meloxicam groups, showing endothelial denudation and intima enlargement from the thoracic aorta in 96% of the slices studied. The decrease in fibrinogen in the meloxicam group would be due to cyclooxygenase-2 (Cox-2) selective inhibition, even though the histopathological lesions did not regress.
Insights
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.