mobic and parecoxib

The dynamics of Parecoxib or Meloxicam analgesic effect on acute postoperative pain was studied in 48 patients (22 female and 26 male) sustaining arthroprosthetic (Parecoxib analgesia) or arthroscopic (Meloxicam analgesia) orthopedic surgery. The results show higher postoperative pain and slower dynamics of Parecoxib and Meloxicam analgesia in women than in men, which necessitates supplementation of the applied analgesic medication in the female patients.

Topics: Adolescent; Adult; Aged; Analgesia; Analgesics; Cyclooxygenase 2 Inhibitors; Female; Humans; Isoxazoles; Male; Meloxicam; Middle Aged; Orthopedic Procedures; Pain, Postoperative; Thiazines; Thiazoles; Young Adult

The purpose of this study was to present the effectiveness of 2 cyclooxygenase-2 inhibitors, meloxicam and parecoxib, in the prevention of heterotopic ossification. Eighteen white mature male rabbits were divided into 3 groups of 6 animals. One was the control group; 1 group was administered meloxicam subcutaneously, and 1 group was administered parecoxib subcutaneously. For the induction of heterotopic new bone, the Michelsson model was used. The extent of heterotopic new bone development was assessed according to Scott's classification. The meloxicam and parecoxib groups developed significantly less heterotopic bone when compared to the control group. There was no significant difference between the meloxicam and parecoxib group. We concluded that meloxicam and parecoxib are capable of preventing the development of heterotopic new bone in rabbits. The clinical relevance of this study is that meloxicam and parecoxib may be helpful in reducing heterotopic ossification in humans.

Topics: Animals; Bone and Bones; Cyclooxygenase 2 Inhibitors; Disease Models, Animal; Indomethacin; Injections, Subcutaneous; Isoxazoles; Male; Meloxicam; Ossification, Heterotopic; Osteogenesis; Rabbits; Radiography; Thiazines; Thiazoles

Kynurenic acid (KYNA), an endogenous glutamate-receptor antagonist preferentially blocking NMDA-receptors, has analgesic properties and has also been implicated in the pathophysiology of schizophrenia. Recently, the non-steroid anti-inflammatory drug (NSAID) diclofenac was found to increase rat brain KYNA. Here, we analyze whether cyclooxygenase (COX)-1 or COX-2 modulate the levels of rat brain KYNA. The non-selective COX-inhibitor diclofenac (50 mg/kg, i.p.) or indomethacin (50 mg/kg, i.p.), a non-selective inhibitor with a preferential selectivity for COX-1, produced an elevation in brain KYNA. In contrast, the COX-2 selective inhibitors parecoxib (25 mg/kg, i.p.) or meloxicam (5 mg/kg, i.p.) decreased brain KYNA. Both elevation and lowering of brain KYNA by indomethacin or parecoxib, respectively, were prevented by the prostaglandin E1/E2 agonist misoprostol (1 mg/kg, s.c.). It is proposed that increased brain KYNA formation induced by NSAIDs displaying an inhibitory action on COX-1 contribute to their analgesic efficacy as well as to their psychiatric side effects.

Topics: Animals; Brain; Diclofenac; Enzyme Inhibitors; Indomethacin; Isoxazoles; Kynurenic Acid; Male; Meloxicam; Prostaglandins; Protein Isoforms; Rats; Rats, Sprague-Dawley; Thiazines; Thiazoles