Flunixin Meglumine Injection Research Articles

DETERIMENTAL EFFECTS OF FLUNIXIN MEGLUMINE ON THE RAT FOETAL DEVELOPEMENT

In pregnant female rat, the cyclooxygenase inhibitor; flunixin meglumine administered intramuscularly in the therapeutic dose and its two fold evoked red patches on different parts of the body. The most frequently observed internal malformations in response to flunixin meglumine injection (0.4 mg/kg B.wt.) were dilated brain ventricles, thickening of the ventricular wall of the heart and dilatation of the renal pelvis. Flunixin meglumine injection at a dose of 0.8 mg/kg B.wt. evoked dilated brain ventricles, cerebral, intrathoracic and abdominal haemorrhages, marked thickening of ventricular wall of the heart and dilatation of renal pelvis. Skeletal malformation or response to both doses of the drug were absence of last caudal vertebrae, pronounced rudimentary or missing sternebrae and xiphisternam and absence of phalanges of both fore and hind limbs.

Flunixin meglumine and flurbiprofen in cows with experimental Escherichia coli mastitis.

The effect of flunixin meglumine and flurbiprofen on the course of experimental Escherichia coli mastitis was examined. Nine cows (within one month post partum) were inoculated intramammarily with 20 x 10(5) viable E coli in both rear quarters. Three cows remained untreated (controls); three cows received three injections of flunixin meglumine and three cows received flurbiprofen as two intravenous infusions. Flunixin meglumine and flurbiprofen were initially given before clinical signs were observed. Treatment was repeated if the cows' temperature increased by more than 1 degree C. In the untreated cows, rectal temperature and heart rate increased from three hours after infection, and rumen motility (both frequency and amplitude) decreased from four hours after infection. Treatment with flunixin meglumine or flurbiprofen almost completely abolished the febrile response during the first nine hours after infection, and the decrease in rumen motility was less pronounced in the treated animals. These results suggest that the decrease in rumen motility during E coli mastitis is at least partly due to a mechanism involving prostaglandin.