Effect of intravenous lidocaine on experimental spinal cord injury.

A series of experiments was conducted to study the effect of systemic intravenous administration of lidocaine on neurological recovery after acute experimental spinal cord injury in cats. The spinal cord was injured by the rapid inflation of an epidural balloon at T-6. The physiological integrity of the spinal cord ceased within 2 seconds in all animals, as demonstrated by acute disappearance of the somatosensory evoked response (SER). There was essentially no return of the SER in the five untreated animals when monitored for 4 hours post-injury. All of the pathological specimens from these animals revealed severe central cord hemorrhage. Intravenous lidocaine was begun 15 minutes after the injury in five animals. Three of these animals had significant return of the SER. The pathological specimens from the lidocaine-treated animals revealed either mild or moderate central cord hemorrhage. The results of this experiment suggest that systemic lidocaine administration has a significant beneficial effect in the treatment of acute spinal cord injury.

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

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.