Abstract
Nitric oxide (NO) is a small, diffusible molecule that plays an important regulatory role in a number of biologic processes involved in ischemic damage: 1) NO has been implicated in vasodilation induced by a variety of vasodilators1; thus, it plays an important role in regulation of tissue perfusion. 2) NO has been implicated in glutamate-mediated neurotransmission via the N-methyl-D-aspartate (NMDA) receptor.2 Thus, NO is linked to the excitotoxic process. 3) NO has been suggested to evoke free-radical tissue damage during postischemic reperfusion.3 In this chapter we summarize a series of studies from our own laboratory, pointing to the role played by NO in excitotoxic and ischemic neuronal damage.