Inhibition of Cerebral Metabolism by Lidocaine

Abstract

The effects of lidocaine in high doses, i.e. higher than seizure doses, on cerebral function and metabolism are reviewed. Evidence is presented that lidocaine (160 mg/kg) reduces membrane NA+-K+ permeability, restricts leak fluxes of these ions, and decreases the load on the associated ion transport. In the ischemic brain (circulatory arrest in dogs on cardiopulmonary bypass circulation), lidocaine delays K+ efflux, indicating reduced membrane permeability. In the nonischemic brain lidocaine has two effects. One is to abolish electrocortical activity and reduce oxygen and glucose consumption accordingly ("barbiturate-like" effect). The other is a specific membrane sealing effect by which Na+-K+ leak fluxes are restricted and associated demand for active transport according reduced. By this effect lidocaine is able to reduce cerebral metabolism by an additional 15-20% below the barbiturate minimum at flat EEG. These effects of lidocaine resemble those of hypothermia and may enhance the hypothermic protection of the ischemic brain.