To the Editor:—

It is well-established that the spinal cord is the predominant site where general anesthetics act to abolish movement in response to painful stimulation. 1–4What is perhaps less well-known is that Claude Bernard 5(1813–1878) had already shown that the spinal cord can be anesthetized independently of the brain.

Bernard used frogs to demonstrate that chloroform acts on the spinal cord 6(an English translation by B. R. Fink is available from the Wood Library-Museum of Anesthesiology, Park Ridge, IL). 6Anesthetic effect was measured as the suppression of reflex limb withdrawal after pinching. The frogs were placed head-down in a vessel filled with a dilute (1:200 in water) solution of chloroform. They were held in place by a rubber membrane. The head and forelimbs of the animal were thus immersed in the anesthetic solution while the hind legs and abdomen remained exposed to air. After a few minutes, the hind legs became anesthetized (as did the forelimbs) as a result of absorption of chloroform through the skin and distribution by blood circulation. Bernard repeated the experiment with a frog whose spinal cord had been cut just below the forelimbs. The hind legs, which at the beginning briskly retracted with pinching, became anesthetized, as seen with a normal frog. Because there was no communication between the brain and the hind legs, Bernard concluded that chloroform is capable of suppressing withdrawal of the pinched limb by acting on the spinal cord alone. (A direct anesthetic effect on nerves had already been ruled out.)

Bernard also showed that anesthetic action on the brain influences the spinal cord. For his demonstration, he ligated the descending thoracic aorta of a frog. After confirming that that pinching of the hind legs still caused withdrawal, he placed the frog head-down in the chloroform solution. The withdrawal reflex was then abolished. He attributed this suppression to an effect of the brain on the spinal cord because the aortic ligature prevented the chloroform from reaching the lower cord.

The foregoing information does not mean that there was no need for the ingenious work of Rampil and Antognini. 1,3,4Experiments with amphibians cannot be blindly applied to mammals. Bernard chose a concentration of chloroform much higher than the ED50(a 1:200 dilution corresponds to 62 mm, whereas the ED50is of the order of 1 mm) 7and did not compare the relative sensitivities of the brain and spinal cord. Finally, he only looked at reflex limb withdrawal to assess anesthetic effect, whereas the recent studies examined gross purposeful movements. 8 

1.
Antognini JF, Schwartz K: Exaggerated anesthetic requirements in the preferentially anesthetized brain. A nesthesiology 1993; 79: 1244–9
2.
Kendig JJ: Spinal cord as a site of anesthetic action. A nesthesiology 1993; 79: 1161–2
3.
Rampil I: Anesthetic potency is not altered after hypothermic spinal cord transection in rats. A nesthesiology 1994; 80: 606–10
4.
Rampil IJ, Mason P, Singh H: Anesthetic potency (MAC) is independent of forebrain structures in the rat. A nesthesiology 1993; 78: 707–12
5.
Leake CD: Claude Bernard and anesthesia. A nesthesiology 1971; 35: 112–3
6.
Bernard C: Leçons sur les anesthésiques et sur l’asphyxie. Paris, Librairie J.-B. Baillière et Fils, 1875, pp 98–132
7.
Firestone LL, Miller JC, Miller KW: Appendix: Tables of physical and pharmacological properties of anesthetics, Molecular and Cellular Mechanisms of Anesthetics. Edited by Roth SH, Miller KW. New York, Plenum Medical Book Company, 1984, pp 455–70
8.
Eger EI, Saidman LJ, Brandstater B: Minimum alveolar anesthetic concentration: A standard of anesthetic potency. A nesthesiology 1965; 26: 756–63