NITRIC-OXIDE AS A MEDIATOR OF INFLAMMATION

The inflammatory process is sustained by synthesis and release of a la rge number of humoral mediators that, in turn, initiate a cascade of s ystemic and local effector molecules in phagocytes (PG) and other soma tic cells. A key position in the cascade process is under the control of the nitric oxide (NO.) pathway activated by injurious agents, cytok ines, and PAF. The activation of the L-arginine-dependent NO. pathway via NO. synthase is an important mechanism of stimulation of both micr obiostatic capability and cytotoxicity of PG. On the other hand, the a ccumulation of nitrosocompounds, NO., NO2-/NO3- in the host tissues is known to produce disruption of immuno-chemical homeostasis, which can result in the endotoxicosis syndrome. In this paper we summarize the available data on the host inflammatory response in its relation to NO . synthesis.