Anesthetic depression of spinal motor neurons may contribute to lack of movement in response to noxious stimuli.

BACKGROUND

Previous studies suggest that anesthetics produce immobility by an action on the spinal cord. We postulated that immobility results from a depression of alpha-motor neuron excitability in vivo, and that this depression would be reflected in a depression of recurrent, (F)-wave activity.

METHODS

The lungs of 15 normocapnic, normothermic, normotensive rats were mechanically ventilated with 0.5, 0.8, 1.2, and 1.6 MAC isoflurane, in random sequence, with at least 30 min of equilibration at each step. In addition, at 1.2 MAC, inspired carbon dioxide was altered to create hypercapnia and hypocapnia. The sizes of the orthodromic (M) wave and F wave were measured in ten sequential trials as the activity in the intrinsic muscles of the ipsilateral foot evoked by stimulation of the tibial nerve.

RESULTS

M-wave amplitude did not change. F-wave amplitude did not decrease between 0.5 and 0.8 MAC but decreased 50% between 0.8 and 1.2 MAC (P < 0.001) and 60% between 1.2 and 1.6 MAC (P < 0.05). Hypocapnia (17 mmHg) increased F-wave amplitude by 15%, and hypercapnia (73 mmHg) reduced it by 60% compared with normocapnia at 1.2 MAC (31 mmHg) (P < 0.0001).

CONCLUSIONS

Anesthetics may cause and moderate hypercapnia may contribute to surgical immobility by depressing excitability of alpha-motor neurons. Monitoring F waves may indicate the adequacy of this aspect of anesthesia and may detect states in which spontaneous or nocifensive movements might occur.