Role of nitric oxide in zymosan induced paw inflammation and thermal hyperalgesia

Abstract

The results show that iNOS is upregulated in the inflamed tissue and spinal cord with a similar time course. The effects obtained with L-NIL suggest that iNOS differently contributes to the inflammatory and nociceptive response induced by zymosan.

Potentiation of diclofenac-induced anti-inflammatory response by aminoguanidine in carrageenan-induced acute inflammation in rats: The role of nitric oxide

“…In contrast, selective inhibition of iNOS by aminoguanidine (AG) had antiinflammatory effects only when it had been administered during late stages of the inflammatory process [13]. The importance of iNOS for the maintenance of acute inflammation is further supported by the observation that its protein expression is upregulated during the late stage of inflammation in paws and in dorsal horn neurons of the spinal cord after injection of carrageenan [2,14]. NO is a potent vasodilator; its involvement during an inflammatory response may be related to its ability to increase vascular permeability and edema through changes in local blood flow [15,16].…”

In vivoanti-inflammatory effect of a sulfated polysaccharide isolated from the marine brown algaeLobophora variegata

“…The paw edema elicited by zymosan shows a biphasic release of NO (early stage) and prostaglandins (late phase) (Damas & Prunesco, 1990). It is also described that the paw edema elicited by zymosan stimulates iNOS messenger RNA expression in a period of 150 min to 24 h after injection (Gühring et al, 2001). Increasing evidence argues in favor of a considerable "cross talk" between the NO and prostaglandins biosynthetic pathways (Weinberg, 2000).…”

The role of reactive oxygen species in capsaicin-induced mechanical hyperalgesia and in the activities of dorsal horn neurons

“…The increased levels of nitric oxide synthase (NOS) and nitric oxide (NO) were observed in the spinal cord after tissue inflammation by capsaicin (Wu et al, 1998;, and this increase is proposed to be a factor that maintains secondary hyperalgesia after capsaicin treatment (Meller and Gebhart, 1993;Wu et al, 1998;. However, when specific and nonspecific NOS inhibitors were used to block pain, the results were inconsistent (Semos and Headley, 1994;Stanfa et al, 1996;Wu et al, 1998;Osborne and Coderre, 1999;Gühring et al, 2001). For example, two inducible NOS (iNOS) inhibitors, aminoguanidine (AG) and 2-amino-5,6-dihydro-methylthiazine (AMT), were effective in reducing carrageenan-induced thermal hyperalgesia (Osborne and Coderre, 1999), but another iNOS inhibitor, L-N6-[1-iminoethyl]lysine (L-NIL), was not effective (Gühring et al, 2001).…”

“…However, when specific and nonspecific NOS inhibitors were used to block pain, the results were inconsistent (Semos and Headley, 1994;Stanfa et al, 1996;Wu et al, 1998;Osborne and Coderre, 1999;Gühring et al, 2001). For example, two inducible NOS (iNOS) inhibitors, aminoguanidine (AG) and 2-amino-5,6-dihydro-methylthiazine (AMT), were effective in reducing carrageenan-induced thermal hyperalgesia (Osborne and Coderre, 1999), but another iNOS inhibitor, L-N6-[1-iminoethyl]lysine (L-NIL), was not effective (Gühring et al, 2001). In other studies, the nonselective NOS inhibitor L-N G -nitro-arginine methyl ester (L-NAME) produced a dose-dependent reduction of carrageenan-induced thermal hyperalgesia (Osborne and Coderre, 1999), but the same drug reduced mechanical hyperalgesia but not thermal hyperalgesia (Semos and Headley, 1994).…”