✓ To evaluate etomidate as a neuroprotective agent in the brain stem, 33 dogs were divided into seven groups and were exposed to isolated, reversible brainstem ischemia in the presence or absence of etomidate using a newly developed canine model of brainstem ischemia. Brainstem auditory evoked potentials (BAEP) and regional cerebral blood flow were measured during ischemia and for 5 hours after reperfusion. This model provides a potential physiological environment in which to test the efficacy of putative brainstem ischemic protective strategies.
During ischemia, BAEP were abolished in all animals. Without etomidate 10 minutes of ischemia was of short enough duration to allow complete recovery of BAEP. Ischemia of 20 or 30 minutes' duration resulted in minimal recovery. The dose of etomidate administered did not suppress BAEP or brainstem cardiovascular response to ischemia. In animals receiving etomidate and rendered ischemic for 20 minutes, a significant but only temporary recovery in BAEP was seen. Etomidate failed to have a significant effect in animals rendered ischemic for 30 minutes.
The minimal effect of etomidate on the current measures of brainstem function is in contrast to etomidate's known suppressive effect on cortical electroencephalogram and predicts that etomidate does little to alter brainstem metabolism. Etomidate's failure to provide for permanent recovery of BAEP suggests that the drug does not give sufficient protection from ischemia to the brainstem neurons in the auditory pathway. If these auditory neurons reflect brainstem function as a whole, etomidate may not be the protective agent of choice during temporary arterial occlusion of posterior circulation.