AbstractOBJECTIVEAugmentation of blood flow to collateral-dependent tissue (CDT) as a result of selective vasodilation of collateral vessels has been shown to occur with various stimuli after middle cerebral artery occlusion. Etomidate, a carboxylated imidazole derivative, is a nonbarbiturate anesthetic that is used clinically both as an anest e ic and as a neuroprotective agent. The effect etomidate has on collateral cerebral vessels is unknown. The purpose of our studies was to test whether etomidate selectively augmented cerebral blood flow (CBF) to CDT du g ischemia as an additional mechanism of neuroprotection.METHODSA left craniotomy was performed in each of 14 dogs, with the animals under halothane anesthesia A branch of the middle cerebral artery was occluded and cannulated distally for determination of CDT using a “shadow flow” technique. CBF and vascular pressures were measured and used to calculate vascular resistance An etomidate infusion (0.1 mg/hg of body weight/min administered intravenously) was started and CBF an vascular pressures were measured at 10 and 40 minutes. Hypotension was then induced, and CBF and pressures were again measured.RESULTSCBF was significantly reduced in all regions of the brain, including CDT, when etomidate was infused CDT showed a 53.7% reduction in flow, whereas normal CBF was reduced by at least 63.4% During hypotension, blood flow to CDT was reduced by an additional 42.7%, whereas normal cerebrum was reduced by at least 22.7%. Vascular resistance was increased in all vessels during etomidate infusion.CONCLUSIONThe neuroprotective effects of etomidate do not seem to be through the augmentation of collateral or global CBF.
Neurosurgery – Oxford University Press
Published: Aug 1, 1998
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