Ketamine suppresses ischemic injury in the rabbit retina.

Overstimulation of the N-methyl D-aspartate (NMDA) receptor has been implicated as a factor in the pathogenesis of ischemic injury in the central nervous system. The present study was undertaken to determine whether ketamine hydrochloride, a potent NMDA antagonist, could attenuate ischemic injury in the rabbit retina. Retinal ischemia was induced for 60 min in one eye of 18 albino rabbits by raising intraocular pressure above the systolic blood pressure. Three concentrations of ketamine, 0.5, 1.5, 5.0 mumol were dissolved in 20 microliters of saline solution and injected in the midvitreous in each eye of 14 rabbits 1 hr prior to ischemia. Four rabbits received saline solution as controls. The scotopic electroretinogram was monitored in each eye to assess the postischemic recovery of retinal function. A statistically significant reduction in the b-wave was detected in the eyes treated with saline (P less than 0.05), whereas the postischemic recovery of b-wave amplitude was enhanced by pretreatment with lower doses of ketamine. The highest dose depressed b-wave amplitude regardless of ischemia. Six rabbits underwent unilateral ocular ischemia under general anesthesia with ketamine. A small ameliorative effect was seen (P = 0.029). These results suggest that ketamine may alleviate ischemic injury in the rabbit retina, presumably by antagonizing the NMDA receptor-mediated toxicity. Thus, ketamine may have potential in the treatment of retinal vascular occlusive diseases. Moreover, a modified ischemic state may exist in experiments on ischemia conducted under general anesthesia with ketamine hydrochloride.