ABSTRACT
A growing body of evidence suggests that the brain damage produced by cerebral ischemia is not as immediate and immutable as previously believed. Although energy failure is rapidly fatal in the center of the ischemic region, in peripheral regions neuronal death follows a slower time-course. The pathogenic processes contributing to the delayed progression of the damage remain, for the most part, obscure. However, recent experimental data indicate that gene products expressed in this region of the ischemic territory play an important role in this process. One such gene product is inducible nitric oxide synthase (iNOS). This enzyme produces toxic amount of NO, a free radical that can act both as a molecular messenger and as a toxin. In this chapter the evidence that iNOS gene expression is involved in the delayed progression of the damage will be examined in the context of the cellular and molecular correlates of cerebral ischemia and neuroprotection.
