Evans D E, Kobrine A I, LeGrys D C, Bradley M E
J Neurosurg. 1984 Feb;60(2):257-63. doi: 10.3171/jns.1984.60.2.0257.
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.
