RT Book, Section
A1 Kelz, Max B.
A1 Todorovic, Slobodan M.
A1 Eckenhoff, Roderic G.
A2 Longnecker, David E.
A2 Brown, David L.
A2 Newman, Mark F.
A2 Zapol, Warren M.
SR Print(0)
ID 56634167
T1 Chapter 37. Mechanisms of General Anesthetic Action
T2 Anesthesiology, 2e
YR 2012
FD 2012
PB The McGraw-Hill Companies
PP New York, NY
SN 978-0-07-178513-6
LK accessanesthesiology.mhmedical.com/content.aspx?aid=56634167
RD 2024/04/19
AB The  mechanisms  by  which  the  inhaled  general  anesthetics  work  are  not  fully  understood.  No  single  molecular  target  has  been  proven  to  transduce  anesthesia.Correlation  of  the  physicochemical  character  of  anesthetics  with  their  potency  suggests  that  target  sites  are  dominantly  hydrophobic,  with  a  small  degree  of  polarity  and  chirality.  Internal  or  interfacial  protein  cavities  best  fit  this  description.Inhaled  anesthetic  binding  site  character  is  not  highly  specific,  predicting  more  than  a  few  anesthetic  binding  targets.  The  interaction  at  some  of  these  targets  may  not  contribute  significantly  to  anesthetic  action  but  may  contribute  to  side  effects.Use  of  the  lipid  membrane  as  a  direct  target  for  inhaled  anesthetics  has  been  dismissed  prematurely.  Some  components  of  anesthetic  action  may  occur  via  this  interaction.Many  potential  protein  targets  in  the  synapse  have  been  identified,  suggesting  that  inhaled  anesthetic  action  results  from  disruption  of  the  specific  process  of  synaptic  transmission  rather  than  from  a  receptor-like  interaction  with  a  single  molecular  target.Anesthetic  effects  on  a  process,  such  as  synaptic  transmission,  may  have  a  different  system-level  effect  depending  on  placement  in  the  neural  circuitry.  The  circuits  that  regulate  sleep  and  arousal  are  well  positioned  to  mediate  the  hypnotic  properties  of  anesthetics.