General anaesthesia: Difference between revisions

The [[biochemistry|biochemical]] [[Theories of general anaesthetic action|mechanism of action of general anaesthetics]] is not well understood.<ref>{{cite journal | vauthors = Jevtovic-Todorovic V | title = General Anesthetics and Neurotoxicity: How Much Do We Know? | journal = Anesthesiology Clinics | volume = 34 | issue = 3 | pages = 439–451 | date = September 2016 | pmid = 27521190 | pmc = 5477636 | doi = 10.1016/j.anclin.2016.04.001 }}</ref> Theories need to explain the function of anaesthesia in animals and plants.<ref>{{cite news| vauthors = Frazier J |title=Plants, Like People, Succumb to Anesthesia|url=https://blogs.scientificamerican.com/artful-amoeba/plants-like-people-succumb-to-anesthesia-video/|access-date=26 January 2018|work=[[Scientific American]]|date=26 January 2018}}</ref> To induce unconsciousness, anaesthetics have myriad sites of action and affect the [[central nervous system]] (CNS) at multiple levels. General anaesthesia commonly interrupts or changes the functions of CNS components including the [[cerebral cortex]], [[thalamus]], [[reticular activating system]], and [[spinal cord]]. Current theories on the anaesthetized state identify not only target sites in the CNS but also [[neural network]]s and arousal circuits linked with unconsciousness, and some anesthetics potentially able to activate specific sleep-active regions.<ref>{{Cite journal |last1=Moody |first1=Olivia A. |last2=Zhang |first2=Edlyn R. |last3=Vincent |first3=Kathleen F. |last4=Kato |first4=Risako |last5=Melonakos |first5=Eric D. |last6=Nehs |first6=Christa J. |last7=Solt |first7=Ken |date=2021-05-01 |title=The Neural Circuits Underlying General Anesthesia and Sleep |journal=Anesthesia and Analgesia |volume=132 |issue=5 |pages=1254–1264 |doi=10.1213/ANE.0000000000005361 |issn=1526-7598 |pmc=8054915 |pmid=33857967}}</ref> Potential molecular pharmacologic targets of general anaesthetics are [[gamma-Aminobutyric acid|GABA_A]],and [[Glutamic acid|NMDA glutamate]] receptors. General anesthesia was hypothesized to either enhance the inhibitory transmission or reduce the excitatory transmission of neuro signaling.<ref>{{Cite journal |last=Lambert |first=David G. |date=2020-05-01 |title=Mechanisms of action of general anaesthetic drugs |url=https://www.anaesthesiajournal.co.uk/article/S1472-0299(20)30028-X/abstract |journal=Anaesthesia & Intensive Care Medicine |language=English |volume=21 |issue=5 |pages=235–237 |doi=10.1016/j.mpaic.2020.02.006 |issn=1472-0299}}</ref> Most volatile anesthetic has been found to be a GABA_A [[agonist]], although the site of action on the receptor remains unknown.<ref>{{Cite journal |last1=Woll |first1=Kellie A. |last2=Zhou |first2=Xiaojuan |last3=Bhanu |first3=Natarajan V. |last4=Garcia |first4=Benjamin A. |last5=Covarrubias |first5=Manuel |last6=Miller |first6=Keith W. |last7=Eckenhoff |first7=Roderic G. |date=August 2018 |title=Identification of binding sites contributing to volatile anesthetic effects on GABA type A receptors |journal=The FASEB Journal |volume=32 |issue=8 |pages=4172–4189 |doi=10.1096/fj.201701347R |issn=0892-6638 |pmc=6044061 |pmid=29505303}}</ref> [[Ketamine]] is a non-competitive [[NMDA receptor antagonist]].<ref>{{Cite journal |last1=Zhang |first1=Youyi |last2=Ye |first2=Fei |last3=Zhang |first3=Tongtong |last4=Lv |first4=Shiyun |last5=Zhou |first5=Liping |last6=Du |first6=Daohai |last7=Lin |first7=He |last8=Guo |first8=Fei |last9=Luo |first9=Cheng |last10=Zhu |first10=Shujia |date=August 2021 |title=Structural basis of ketamine action on human NMDA receptors |url=https://pubmed.ncbi.nlm.nih.gov/34321660 |journal=Nature |volume=596 |issue=7871 |pages=301–305 |doi=10.1038/s41586-021-03769-9 |issn=1476-4687 |pmid=34321660|bibcode=2021Natur.596..301Z |s2cid=236496390 }}</ref>

 

 

== Preoperative evaluation ==