ABSTRACT
One can reasonably predict that NO will promote cellular dysfunction and tis sue injury only when it is produced in large amounts, and this invariably requires the expression of the inducible form of nitric oxide synthase (iNOS). If iNOS is absent, then NO will primarily exhibit anti-inflammatory effects (1). Conversely, the presence of iNOS is an excellent indicator that NO is directly contributing to cellular injury (2). The best exception for this “rule” is pregnancy, and the possible explanations for this exception are discussed at the end of the chapter. Infection, where the high rate of NO production is necessary for the clearance of the infection, is also a state where the contribution of NO to tissue injury must be tempered by the pathology of the infection itself. Under these conditions NOS inhibition may exacerbate or hinder the pathology depending on the relative strengths of the host defense response versus the aggressiveness of the invading micro-organism (3).
