An Experimental Model of Brain Ischemia Combining Hypotension and Hypoxia

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Abstract
A variety of experimental models for cerebral ischemia are currently available, but none are entirely satisfactory. We are reporting a model which combines hypotension, produced by intravenous Arfonad, with hypoxia, produced by respiring 4% oxygen. Rabbits used are awake but paralyzed with succinylcholine and ventilated mechanically. The electroencephalogram (EEG) is monitored with durally implanted electrodes. Onset of an isoelectric EEG ensues 4.5 ± 0.7 minutes in 17 rabbits studied and is used to measure the degree of ischemic insult. After three minutes of an isoelectric EEG, circulatory restoration is followed by complete functional recovery. After five minutes of an isoelectric EEG, rabbits do not recover or show neurological deficits such as limb weakness. The potential effects of systemic ischemia on these animals are minimized because of the rapid onset of ischemic brain damage. Examination of arterial blood gases, pH, platelets, various organs histologically, and the distribution of carbon-particles in the intracerebral circulation reveals that systemic factors are minimal. Moderately delayed onset of cortical EEG activity and the presence of motor impairment or an inability to respire satisfactorily after extubation indicates that the brunt of ischemic insult is upon brain. Our model has the advantages of simplicity and predictability and offers the opportunity to assess functional impairment after graded degrees of cerebral ischemia. We conclude that our model of cerebral ischemia produced by hypotension and hypoxia is a reasonable alternative to existing methods.