Wednesday, May 2, 2018

Need to know how does Anesthesia work?

General anesthesia is the sum of hypnosis (sleep), amnesia, analgesia (pain relief), and
the lack of any motion response to pain. Propofol and barbiturates cause hypnosis. Versed
and other benzodiazepines cause amnesia. Narcotics such as morphine and fentanyl cause
analgesia. Paralyzing drugs such as rocuronium, vecuronium, and succinylcholine cause
muscle relaxation and lack of motion.The potent inhaled anesthetics sevoflurane, desflurane,
and isoflurane produce all four of the effects of hypnosis, Anesthesia journal amnesia,
analgesia, and lack of motion.


The molecules of anesthetic drugs have great diversity. Some are very small, such as
nitrous oxide, while others such as propofol or barbiturates have complex formulas. Some
are gases and some are injected liquids. This diversity leads investigators to postulate that
there are multiple mechanisms of action for anesthetic drugs on the brain.




Drugs such as propofol and Versed are injected into the bloodstream and are circulated to
the central nervous system, where they carry out their effect on brain cells. Inhaled
anesthetics such as sevoflurane and desflurane traverse from the lungs into the bloodstream
and are circulated to the central nervous system, where they carry out their effect on brain cells.


Once in the brain, it’s not clear how Anesthesia journal anesthetic drugs work. Most anesthetic drugs are hydrophobic, which literally translates to
“water-fearing.” This means their molecules are more soluble in fat than in water. Anesthetic
drugs exhibit a correlation between their potency and how hydrophobic they are. The entry
of any drug into a brain cell must be via the outer lining, or membrane, of that cell. Investigators
believe anesthetics must move through, or bind to, the fat-soluble aspects of the membranes
of brain cells. The drugs likely then bind to proteins within the cell membranes and cause
their anesthetic effect by changing the characteristics of ion channels within the cell
membranes. There is no unifying theory as to how this occurs, but it is known that anesthetic
agents have effects on brain cell membrane proteins, which depend on the hydrophobic,
electrostatic, and size properties of the individual drug.


Specific examples in our understanding of anesthetic actions include:

1.Barbiturate drugs, propofol, and inhalational anesthetics are known to act by potentiating a
brain chemical called gamma-aminobutyric acid, or GABA. GABA is an inhibitory neurotransmitter,
meaning it’s a brain chemical which inhibits other brain activity. This inhibition in some way
promotes unconsciousness.
2.The anesthetics nitrous oxide and ketamine are known to antagonize an excitatory N–
methyl-d-aspartate (NMDA) subtype of neurotransmitter. By blunting this excitatory process,
the drugs work to promote unconsciousness.



The takeaway message is that no Gastroenterology journal specific premise exists to
explain how all the different general anesthetic drugs work on the brain. A variety of mechanisms
likely results in similar effects on the brain, each eliminating the transmission of sensory
messages to the brain and initiating unconsciousness.Anesthesiologists administer other
types of drugs, including narcotics, paralyzing drugs, and local anesthetics. The mechanisms
of action of these medications are better understood.

Narcotics such as morphine, fentanyl, Demerol, or Dilaudid cause pain relief by binding to
opioid receptors in the brain (or the spinal cord). The most common narcotic side effects,
e.g. sleepiness and nausea, also arise from the direct effect of the narcotics on the brain.
Narcotics bind to three specific receptors in the central Gastroenterology journal nervous system: the mu, delta, and kappa receptors. The receptor is primarily responsible
for the pain-relieving and euphoria-inducing effects of narcotics. Investigators are searching
for new narcotics to specifically target the receptor, with the aim of reducing side effects of
sedation and nausea.

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