(Fig. 5-3: A multisite model for anesthesia)
- It is clear that all anesthetic actions cannot be localized to a specific anatomic site in the CNS. (Considerable evidence supports the conclusion that different components of the anesthetic state are mediated by actions at disparate anatomic sites.)
- The actions of anesthetics cannot be localized to a single physiologic process.
- At a molecular level, volatile anesthetics show some selectivity but still affect the function of multiple ion channels and synaptic proteins.
- The intravenous anesthetics, etomidate, propofol, and barbiturates are more specific with the GABAA receptor as their major target.
- Genetic data plainly demonstrate that the unitary theory of anesthesia is not correct.
- No single mechanism is responsible for the effects of all general anesthetics, nor does a single mechanism account for all of the effects of a single anesthetic, at least where it has been examined.
- The precise set of molecular interactions responsible for producing anesthesia have not been fully elucidated, but anesthetics do act via selective effects on specific molecular targets.