Hyperfibrinogenemia in rats treated with meloxicam.
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| 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.
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| Authors | Mónica Moya, Vilma Campana, Antonio Gavotto, L Spitale, Juan Simes, José Palma |
| Journal | Japanese heart journal (Jpn Heart J) Vol. 43 Issue 5 Pg. 559-66 (Sep 2002) ISSN: 0021-4868 [Print] Japan |
| PMID | 12452313 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't) |
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