The b-wave of the electroretinogram (ERG) is a particularly sensitive index of retinal ischemia. The present paper summarizes the changes in the b-wave observed in five in vivo models of retinal ischemia. 2. Although the amount of reduction in b-wave amplitude during ischemia corresponds to the severity of the insult, the degree of recovery of the b-wave during reperfusion depends on the duration of ischemia. 3. A massive release of glutamate, intracellular overload with calcium and enhanced production of free radicals are suggested to be three major pathophysiological processes that contribute to retinal ischemic damage. The b-wave of the ERG represents a functional measure for potential therapeutic efficacy of drugs interacting with these pathophysiological processes. 4. Several glutamate antagonists, such as MK-801, memantine, flupirtine or GYKI 52466, along with the free radical scavengers vitamin E, lipoate, superoxide dismutase and catalase, all reduce the depression of the b-wave during ischemia or accelerate the recovery of the b-wave during reperfusion or both. The calcium channel antagonists nimodipine and levemopamil exert only a slight beneficial effect on the recovery of the amplitude of the b-wave during reperfusion, provided that the blood pressure is not potently reduced.
