Intravenous Anesthetic

Intravenous anesthetic acts primarily at the GABA receptors producing hyperpolarizaztion of the nerve cell membrane. Benzodiazepenes, thiopental, propofol and etomidate bind modulator sites of the GABA A subtype receptors enhancing the inhibitory effect of these neurons. Unlike other intravenous anesthetic, ketamine depresses CNS activity by suppressing excitatory signals mediated by L-glutamate on NMDA receptor channels.

Inhalational Anesthetics

The molecular physiology of inhalational anesthetics is not completely understood with several hypotheses explaining anesthetic and channel interactions. The volume expansion hypothesis proposes that the anesthetics enter lipid membranes and create lateral pressure on channels preventing the influx of ions. The membrane fluidization hypothesis proposes that the anesthetic increases membrane protein motility and disrupts the arrangement of membrane lipid molecules causing ionic channels to lose their structural support and function. The protein interaction hypothesis proposes a direct action of inhalational anesthetics on amphophillic channel proteins thus modulating their gating mechanisms (Table 4.1).

Local Anesthetics

Local anesthetics also are felt to interact with membrane receptors in multiple different ways. The membrane receptor hypothesis states that local anesthetics enter the axon as uncharged bases, gain a charge forming acids which then bind receptor sites in sodium channels that prevent depolarization and impulse propagation. The membrane expansion hypothesis states that uncharged molecules such as benzocaine dissolve in the lipid matrix of the cell membrane allowing these membranes to expand and compress sodium channels thus blocking the passage of sodium ions, preventing subsequent depolarization. The surface charge hypothesis postulates that

Table 4.1. inhalational anesthetic characteristics


Minimum Alveolar Concentration


Nitrous oxide Halothane Isoflurane Enflurane

Analgesic with little respiratory or cardiac depression. Slow uptake and elimination; cardiac depression; uterine relaxation Muscle relaxation; stable cardiac; neurosurgical application Muscle relaxation; seizure activity

positively charged anesthetics bind to the axonal membrane making the external surface more positive than the internal surface thus hyperpolarizing the axonal membrane.

Muscle Relaxants

Muscle relaxants act directly on the motor endplate acetylcholine channels.

Nondepolarizing muscle relaxants are acetylcholine analogues that are competitive inhibitors binding reversibly with ligand gated channels preventing their activation by acetylcholine. As the concentration of relaxant molecules increases the population of functioning ion channels declines. When sufficient numbers of receptors are occupied, action potentials fail to propagate producing muscle relaxation. Nondepolarizing muscle relaxants also block access of acetylcholine to prejunctional receptors interfering with the mobilization of this neurotransmitter.

Depolarizing muscle relaxants have agonist activities at acetylcholine receptors causing prolonged depolarization of the motor end plate, interrupting neuromuscu-lar signal transmission.


Opiates act on the body's natural anesthetic pathways as analogues of the en-kephalins and the endorphins at opioid receptors. There are five species of opioid receptor including the mu, delt, kappa, sigma and epsilon receptors. The opioids act primarily as agonists on the mu receptors producing symptoms of analgesia and euphoria.

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