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General anesthesia likely involves inhibition of the opening of the ion channel in a

postsynaptic ligand-gated membrane protein. Calculations yield qualitative

agreement with anesthetic potency at clinical anesthetic membrane concentrations

and predict the alkanol cutoff and anomalously low potencies of strongly hydrophobic

molecules with little or no attraction for the aqueous interface, such as

perfluorocarbons.

It was shown that anaesthetics alter the functions of many cytoplasmic

signalling proteins, including protein kinase C. They bind directly only

to small number of targets in CNS mostly ligand (neurotransmitter)

gated ion channels in synapse and !protein coupled receptors alteringtheir ion "u#.

Se$o"urane, iso"urane, propofol. Immobility and cerebral e%ects

re"ect di%erent entities of anaesthetic action. &'C (&inimum 'l$eolar

Concentration of inhaled anaesthetic) concentration of the $apor in the

lungs that is needed to pre$ent mo$ement (motor response) due to

surgical stimulus, used to compare strengths or potency of anaesthetic

$apor. 'lthough &'C may not ha$e re$ealed information on the

cerebral sites of anesthetic action and anesthetic actions on sensory

processing, one of the great benets of the &'C studies was to denea set of drug concentrations that are appropriate to induce anesthesia.

C*+i minimum plasma concentration of intra$enous anaesthetic

(nonopioid)

-tomidate, midaolam, propofol (lipolik), thiopental. -nhancing the

acti$ity of inhibitory neurotransmitter yaminobutyric acid (!'/') in

the central neuron system. 0etamine, nitrous o#ide and #enon inhibit

ionotropic glutamate receptors, with the strongest e%ects being seen

on the N&1' receptor subtype. 0etamine antagonies the e%ect of the

e#citatory neurotransmitter Nmethyl1aspartate (N&1') on its

receptors. 2pioid agonists stimulate opioid receptors. !eneral

anesthetics also ha$e a spectrum of modest to strong e%ects on other

ion channels, including glycine receptors, neuronal nicotinic receptors,

*3T4 receptors, glutamate receptors and the two pore potassium

channels. These drugs ha$e rapid action and 5uickly cleared from the

bloodstream and CNS, facilitating control of anaesthetic state (tirtration

e%ect). It also protects $ital tissue, memiliki efek yg lebih ringan, tidak

mempengaruhi sistem peredaran darah atau mengakibatkan efek

samping lainnya. /ereaksi di otak, ber6alan dari tempat in6eksi, kurang

lebih 7 menit. Tidak larut dalam darah dan langsung dibersihkan di hati

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 The transmittergated ion channel (T!IC) superfamily and includes g

aminobutyric acid type ' (!'/''), strychninesensiti$e glycine,

neuronal nicotinic acetylcholine (n'ch) and *hydro#ytryptamine (*

3T4) receptors. 'cti$ation of !'/'' receptors induces inward

mo$ement of mainly chloride ions down their electrochemical gradient

resulting in a hyperpolariation of the cell membrane, whereas

acti$ation of nicotinic receptors produces a net inward mo$ement of

sodium ions and depolariation of the cell membrane. Therefore,

augmenting an inhibitory signal, or inhibiting an e#citatory signal,

pro$ides a logical mechanism for general anaesthetic action

8seful e%ects of general anaesthetic include unconsciousness,

analgesia, suppression of autonomic re"e#es (increasing blood

pressure, and heart rate), and muscle rela#ation. &o$ement re"ects a

shallow depth of anesthesia and can interfere surgery.

!eneral anestesi adalah proses mendapatkan suatu keadaan otak yang

tidak sadar. Namun 6ika hanya tidak sadar, surgical stimulus yang

didapatkan pasien dapat mengakibatkan awakening. 8ntuk mencegah

awakening maka stimulus tersebut di inhibisi agar tidak sampai ke

otak. 3al ini dilakukan dengan menghambat ker6a reseptor opioid disaraf perifer.

't the cellular le$el, anesthetics alter the beha$ior of neurons, by

interacting directly with a small number of ion channels. 8nder normal

conditions, these specialied membrane proteins are acti$ated by

chemical signals or changes in the membrane en$ironment. 8pon

acti$ation, channels change the electrical e#citability of neurons by

controlling the "ow of depolariing (e#citatory) or hyperpolariing

(inhibitory) ions across the cell membrane via an ion channel that isintegral with the receptor that senses the initial signal. General

anesthetics primarily act by either enhancing inhibitory signals or by

blocking excitatory signals.

'nalgesic fentanyl, sufentanil, alfentanil, remifentanil. 3ypnotic

iso"urane, des"urane,se$o"urane, propofol. Inhibit ker6a enim, inhibit

ion channel, inhibit pelepasan neurotransmitter, dan inhibit protein

reseptor di terminal post sinaps