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Correspondence  |   December 1995
Unitary Versus Multiple Mechanisms of Anesthesia
Article Information
Correspondence   |   December 1995
Unitary Versus Multiple Mechanisms of Anesthesia
Anesthesiology 12 1995, Vol.83, No Pagination Specified. doi:
Anesthesiology 12 1995, Vol.83, No Pagination Specified. doi:
To the Editor:--The discussions in the report by Ichinose et al. 1and in the accompanying editorial by Johns 2may be misinterpreted. Both argue that the data support the idea that "multiple pathways are responsible for anesthesia" 2or "for maintaining pain perception and consciousness." 1We have no quarrel with either this generalization or the elegant study by Ichinose et al. that supports it. However, the notion of multiple pathways might be interpreted to mean that several mechanisms in concert (perhaps involving several molecular sites of inhaled anesthetic action) are responsible for the phenomenon of anesthesia (or pain perception and consciousness). An alternative view (one we prefer) is that there is one mechanism for each of these phenomena and one molecular site of action for such phenomena but that other factors (e.g., temperature, 3hyperbaric conditions, 4altered transmitter release 5) also can influence each site. A particularly pertinent example is the decrease in minimum alveolar concentration resulting from ablation of brainstem nuclei 6: Although the brainstem nuclei can influence minimum alveolar concentration, the capacity of inhaled anesthetics to abolish movement in response to noxious stimuli is mediated by an effect on the spinal cord rather than the brainstem. 7-9.
The difference between one versus multiple mechanisms for a given anesthetic endpoint is more than semantic or trivial. The multiple mechanisms notion is complex and may not be testable. The notion of a single mechanism is parsimonious and testable.
Edmond I. Eger II, M.D., Donald D. Koblin, Ph.D., M.D., Department of Anesthesia, Box 0464, Science-455, University of California, San Francisco, 513 Parnassus Avenue, San Francisco, California 94143–0464.
REFERENCES
Ichinose F, Huang P, Zapol W: Effects of targeted neuronal nitric oxide synthase gene disruption and nitro sup G -L-arginine methylester on the threshold for isoflurane anesthesia. ANESTHESIOLOGY 83:101-108, 1995.
Johns R: Nitric oxide and minimum alveolar concentration: TKO or knockout? ANESTHESIOLOGY 83:6-7, 1995.
Eger EI II, Saidman L, Brandstater B: Temperature dependence of halothane and cyclopropane anesthesia in dogs: Correlation with some theories of anesthetic action. ANESTHESIOLOGY 26:764-770, 1965.
Kent D, Halsey M, Eger EI II, Kent B: Isoflurane anesthesia and pressure antagonism in mice. Anesth Analg 56:97-101, 1977.
Johnston R, White P, Eger EI II: Comparative effects of dextroamphetamine and reserpine on halothane and cyclopropane anesthetic requirements. Anesth Analg 54:655-659, 1975.
Roizen M, White P, Eger EI II, Brownstein M: Effects of ablation of serotonin or norepinephrine brain-stem areas on halothane and cyclopropane MACs in rats. ANESTHESIOLOGY 49:252-255, 1978.
Rampil I, Mason P, Singh H: Anesthetic potency (MAC) is independent of forebrain structures in the rat. ANESTHESIOLOGY 78:707-712, 1993.
Antognini J, Schwartz K: Exaggerated anesthetic requirements in the preferentially anesthetized brain. ANESTHESIOLOGY 79:1244-1249, 1993.
Rampil I: Anesthetic potency is not altered after hypothermic spinal cord transection in rats. ANESTHESIOLOGY 80:606-610, 1994.