Protective effect of lidocaine in acute cerebral ischemia induced by air embolism

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✓ To investigate possible approaches to the prevention and treatment of neural damage induced by air embolism and other forms of acute cerebral ischemia, a model was used in which cerebral air embolism was produced by infusion of air (0.4 ml) into a vertebral artery of chloralose-anesthetized cats. Neurological function was assessed by measuring cortical somatosensory evoked responses in a group of 10 untreated animals and in a group of eight animals pretreated with intravenous lidocaine (5 mg/kg). In the untreated group, the primary somatosensory amplitude was reduced to 28% ± 9% (mean ± standard error) of the value before air embolism, with a return to 60% ± 8% 1 hour and 73% ± 12% 2 hours after embolism. In the group pretreated with lidocaine, the primary somatosensory amplitude was reduced to 68% ± 9% of the value before air embolism, with a return to 92% ± 3% 1 hour and 97 ± 2% 2 hours after embolism. Pretreatment with lidocaine also greatly attenuated the acute hypertension and the increase in intracranial pressure following air embolism. These results demonstrate that pretreatment with intravenous lidocaine significantly reduces the neural decrement and increases the recovery of neural function after acute cerebral ischemia induced by air embolism.

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Address reprint requests to: Delbert E. Evans, Ph.D., Naval Medical Research and Development Command, Naval Medical Command, National Capital Region, Bethesda, Maryland 20814.

© AANS, except where prohibited by US copyright law.

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Figures

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    The effect of cerebral air embolism on the primary (left) and secondary (right) somatosensory evoked responses in untreated and lidocaine-pretreated animals. Values are means ± standard error.

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    The percent of animals in untreated and lidocaine-pretreated groups that recovered greater than 90% of somatosensory evoked responses after cerebral air embolism.

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    The effect of air embolism on somatosensory evoked response latency (time from stimulus to time of primary peak) in untreated and lidocaine-pretreated groups.

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    The effect of a second infusion of air into the cerebral circulation, given 2 hours after the first, on the primary somatosensory evoked responses in untreated and lidocaine-pretreated animals.

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    The effect of cerebral air embolism on heart rate and mean blood pressure (left), and intracranial pressure (right) in untreated and lidocaine-pretreated animals. All measurements were made at 20-second intervals.

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