Raws li kev txhawb nqa tseem ceeb rau kev kho mob perioperative, cov txheej txheem ntawm kev txiav txim ntawm cov khoom siv tshuaj loog yog ua raws li kev sib koom tes ntawm neuroscience, pharmacology, thiab physiology.Lawv tsom mus cuam tshuam rau kev xa cov paj hlwb thiab lub cev reflexes los ntawm cov khoom tshwj xeeb lossis cov thev naus laus zis, yog li ua tiav ntau lub hom phiaj ntawm kev tsis nco qab, txo qis kev ntxhov siab. Kev nkag siab tob txog lawv cov txheej txheem ntawm kev ua haujlwm tsis yog tsuas yog pab txhim kho cov txheej txheem kho mob nkaus xwb tab sis kuj muab lub hauv paus theoretical rau kev txhim kho thiab kev nyab xeeb ntawm cov khoom siv tshuaj loog tshiab.
Cov hauv paus ntsiab lus ntawm cov khoom siv tshuaj loog feem ntau yog nyob ib ncig ntawm qhov thim rov qab inhibition ntawm lub hauv paus paj hlwb. Intravenous anesthetics (xws li propofol thiab barbiturates) txhim khu GABA-mediated inhibitory neurotransmission los yog inhibit qhov kev ua ntawm excitatory amino acid (xws li glutamate) receptors, txo cov excitability ntawm lub paj hlwb cortex thiab thalamus, yog li inducing sedation, los yog txawm hypnosis. Inhaled tshuaj loog (xws li sevoflurane thiab isoflurane) diffuse mus rau hauv cov hlab ntsha cell membranes vim lawv cov lipid solubility thiab siab affinity rau paj hlwb, hloov ion channel conformation thiab neurotransmitter tso tawm qauv, yog li inhibiting central integrative muaj nuj nqi. Lub synergistic nyhuv ntawm inhaled tshuaj loog thiab isoflurane tswj qhov tob ntawm cov tshuaj loog nyob rau hauv kev phais, thaum tswj induction thiab awakening los ntawm regulating alveolar concentration thiab intracranial ib nrab siab.
Cov tshuaj loog hauv zos ua haujlwm ntawm lub hauv paus ntsiab lus ntawm peripheral paj conduction blockade. Feem ntau siv tshuaj (xws li lidocaine thiab ropivacaine) khi rau qhov hluav taws xob-gated sodium channels ntawm cov hlab ntsha fiber ntau, tiv thaiv sodium ion influx thiab inhibiting kev tsim muaj peev xwm thiab kev coj ua, yog li thaiv kev sib kis ntawm qhov mob, kub, thiab tactile signals ntawm qhov chaw txhaj tshuaj. Lawv qhov ntau ntawm kev ua yog nyob ntawm cov tshuaj concentration, ntau npaum li cas, thiab qhov chaw txhaj tshuaj; siab concentrations yuav ua rau lub cev muaj zog hlab ntsha blockade, thaum uas tsis muaj concentrations khaws cia lub cev muaj zog muaj nuj nqi, ua tau raws li cov kev xav tau kev kho mob sib txawv. Tsis tas li ntawd, qhov sib txawv ntawm lipid solubility ntawm cov tshuaj loog hauv zos cuam tshuam rau lawv qhov diffusion thiab lub sijhawm, muab lub hauv paus rau kev xaiv tus kheej ntawm cov txheej txheem phais thiab cov tshuaj tua kab mob.
Lub mechanism ntawm kev txiav txim ntawm cov leeg nqaij relaxants yog ywj siab ntawm kev nco qab thiab mob modulation. Lawv feem ntau ua tiav cov leeg pob txha so los ntawm kev cuam tshuam nrog cov teeb liab kis tau tus mob ntawm qhov sib txuas neuromuscular. Depolarizing nqaij relaxants (xws li succinylcholine) ua raws li qhov kev txiav txim ntawm acetylcholine, tsis tu ncua activating nicotinic acetylcholine receptors, ua rau tsis tu ncua daim nyias nyias depolarization thiab ua rau cov leeg tuag tes tuag taw. Tsis yog -depolarizing cov leeg nqaij so (xws li vecuronium thiab rocuronium) sib tw tuav cov receptors, tiv thaiv acetylcholine binding thiab yog li cuam tshuam cov hlab ntsha impulse- induced contractions. Cov tshuaj no tsuas yog siv ua ke nrog cov tshuab ua pa thiab yuav tsum tau siv ua ke nrog cov koob tshuaj txaus ntawm cov tshuaj sedatives thiab tshuaj tua kab mob kom tiv thaiv kev ua haujlwm tsis zoo thiab tsis xis nyob.
Lub hauv paus ntsiab lus ntawm adjunctive anesthetic tshuaj yog kom optimize tag nrho cov tshuaj loog nyhuv thiab txo cov kev phiv tshwm sim. Opioid analgesics (xws li fentanyl thiab sufentanil) activates μ receptors, inhibiting mob kis kab mob nyob rau hauv tus txha caj qaum thiab hlwb, tsa qhov mob pib, thiab txo qis cov tshuaj hormones. Alpha₂ receptor agonists (xws li dexmedetomidine) ua rau ntawm qhov chaw coeruleus, tsim cov tshuaj sedative, anxiolytic, thiab sympathetic inhibitory teebmeem, muab qhov zoo ntawm stabilizing ncig thiab txo cov tshuaj loog. Anticholinergic tshuaj thaiv M receptors, inhibiting glandular secretion thiab vagal reflexes, ua kom cov pa hauv nruab nrog cev thiab lub plawv dhia stability.
Cov khoom siv tshuaj loog niaj hnub kuj suav nrog kev saib xyuas thiab kev tawm tswv yim mechanisms. Electroencephalography (EEG) kev saib xyuas (xws li BIS thiab entropy index) ntsuas qhov tob ntawm cov tshuaj loog los ntawm kev txheeb xyuas cov yam ntxwv ntawm cortical hluav taws xob, muab lub hauv paus rau kev kho tshuaj ntau npaum li cas. Kev saib xyuas cov leeg nqaij so ntsuas ntsuas qib ntawm kev thaiv raws li qhov txo qis ntawm cov hlab ntsha peripheral stimulation- ntxias cov lus teb, coj lub sij hawm ntawm cov leeg nqaij relaxant discontinuation. Kev siv cov hauv paus ntsiab lus no hloov cov tshuaj loog los ntawm kev paub dhau los- tau tsav mus rau kev tswj kom meej, txo cov kev pheej hmoo xws li kev paub txog kev ua haujlwm hauv lub cev, kev hloov pauv hauv lub cev, thiab kev puas siab puas ntsws tom qab phais.
Zuag qhia tag nrho, cov txheej txheem ntawm kev ua ntawm cov khoom siv tshuaj loog yog ua raws li cov kev cuam tshuam ntawm cov neurofunctional reversible, tsim kom muaj kev nyab xeeb, tsis mob, thiab cov leeg nqaij - so kom txaus rau cov txheej txheem phais thiab kev tswj xyuas qhov tseem ceeb los ntawm kev sib koom ua ke ntawm ntau lub hom phiaj thiab cov txheej txheem. Nrog rau txoj kev loj hlob ntawm molecular pharmacology thiab neuromodulation tshuab, kev tshawb fawb rau hauv nws cov hauv paus ntsiab lus yuav txuas ntxiv mus tob, tsav cov khoom siv tshuaj loog mus rau ntau dua precision thiab tus kheej.