Modulation of morphine antinociception in the mouse by endogenous nitric oxide.

1. L-Arginine (100-1000 mg kg-1) administered orally (p.o.) or intraperitoneally (i.p.), but not intracerebroventricularly (i.c.v., 0.08 mg per mouse), reduced the antinociceptive effect of morphine (0.5-10 mg kg-1 s.c.) assessed in mice using three different tests: hot plate, tail-flick and acetic acid-induced writhing. D-Arginine (up to 1000 mg kg-1 p.o. or i.p.) was ineffective. 2. NG-Monomethyl-L-arginine (L-NMMA, 5-50 mg kg-1 i.p.) and NG-nitro-L-arginine methyl ester (L-NAME, 5- 30 mg kg-1 i.p.), but not NG-nitro-D-arginine methyl ester (D-NAME, 30 mg kg-1 i.p.), reversed in all assays the effect of L-arginine on morphine-induced antinociception. 3. Morphine (10 mg kg-1 s.c.), L-arginine (1000 mg kg-1 p.o.) or L-NAME (30 mg kg-1 i.p.), either alone or in combination, did not produce changes in locomotor activity or sensorimotor performance of animals. 4. These results suggest that the L-arginine-nitric oxide pathway plays a modulating role in the morphine-sensitive nociceptive processes.

[Drug-induced gingival proliferation: overview of etiology and treatment]. / La prolifération gingivale d'origine médicamenteuse: aperçu de l'étiologie et du traitement.

Cyclosporine, substituted Dihydropyridines and Phenytoin are three drugs that are often correlated with gingival overgrowth. Differences in incidence and histology are reviewed. Due to the large range of illnesses for which these drugs are prescribed, we can only anticipate a high increase in the number of patients who seek treatment for their enlarged gums. Contemporary treatment modalities are changing towards increased usage of these pharmaceutics which will lead to a high frequency of patients which have drug induced alterations of their gingival structures. The dental practitioners will also need to be consulted prior to drug treatment so that preventive measures can be taken. Treatment of gingival overgrowth is discussed.

Hyaluronic Acid inhibits polycation induced cellular responses.

Positively charged macromolecules cause a variety of pathological events through their electrostatic interaction with anionic sites present on the membrane of target cells. In the present study we have investigated the effect of hyaluronic acid, a negatively charged molecule, on rat paw oedema induced by poly-L-lysine as well as on histamine release from rat mast cells and nitric oxide formation from rabbit aorta, both induced by this polycation. The results indicate that hyaluronic acid is able to suppress these poly-L-lysine induced effects with a mechanism which possibly depends on its negative charges which may balance the effects of positively charged polycations.