Further proof that the spinal cord, and not the brain, mediates the immobility produced by inhaled anesthetics

Previous investigations indicate that the spinal cord, perhaps with a minor cerebral contribution, mediates the capacity of inhaled anesthetics to produce immobility in the face of noxious stimulation. The implications of these investigations may be limited by the trauma associated with their experimental methods (e.g., cardiopulmonary bypass or transection of the spinal cord). The present study avoided such trauma.

Thirty goats received emulsified isoflurane via either the initial section of the aorta (arterial group; preferential isoflurane delivery to the spinal cord) or an ear vein (venous group; equal delivery of isoflurane to the cord and brain). The authors determined the minimum partial pressure of isoflurane (the isoflurane partial pressure in the blood required to produce immobility in 50% of the goats exposed to a noxious stimulus).

For the venous group, the minimum partial pressure in carotid versus femoral arterial blood (9.56 +/- 1.86 mmHg vs. 9.68 +/- 1.90 mmHg) did not differ. For the arterial group, the minimum partial pressure in carotid arterial blood was half that in femoral arterial blood (5.35 +/- 1.45 mmHg vs. 10.97 +/- 3.04 mmHg, P < 0.05). As these data show, the minimum partial pressure in femoral arterial blood did not differ for the arterial group versus the venous group.

In this novel and minimally traumatic model, the anesthetic partial pressure delivered to the spinal cord governed the suppression of movement in response to noxious stimulation. The results indicate that the spinal cord is the primary mediator of immobility and that the brain plays little or no role.