Sedative: Difference between revisions
Jump to navigation
Jump to search
imported>Robert Badgett |
imported>David E. Volk (subpages and wikilinks) |
||
| Line 1: | Line 1: | ||
{{subpages}} | |||
==Classification== | ==Classification== | ||
Below are examples of available sedative drugs. | Below are examples of available sedative drugs. | ||
===Alcohols=== | ===Alcohols=== | ||
====Ethylene glycols==== | ====Ethylene glycols==== | ||
* Chloral hydrate | * [[Chloral hydrate]] | ||
===Anti-adrenergics=== | ===Anti-adrenergics=== | ||
Inhibitors of the adrenergic alpha-2 receptor can cause sedation. | Inhibitors of the adrenergic alpha-2 receptor can cause sedation. | ||
* Dexmedetomidine. In some settings, dexmedetomidine may cause less [[adverse drug reaction]]s than non-selective benzodiazepams.<ref name="pmid18073360">{{cite journal |author=Pandharipande PP, Pun BT, Herr DL, ''et al'' |title=Effect of sedation with dexmedetomidine vs lorazepam on acute brain dysfunction in mechanically ventilated patients: the MENDS randomized controlled trial |journal=JAMA |volume=298 |issue=22 |pages=2644–53 |year=2007 |pmid=18073360 |doi=10.1001/jama.298.22.2644}}</ref> | * [[Dexmedetomidine]]. In some settings, dexmedetomidine may cause less [[adverse drug reaction]]s than non-selective [[benzodiazepam|benzodiazepams]].<ref name="pmid18073360">{{cite journal |author=Pandharipande PP, Pun BT, Herr DL, ''et al'' |title=Effect of sedation with dexmedetomidine vs [[lorazepam]] on acute brain dysfunction in mechanically ventilated patients: the MENDS randomized controlled trial |journal=JAMA |volume=298 |issue=22 |pages=2644–53 |year=2007 |pmid=18073360 |doi=10.1001/jama.298.22.2644}}</ref> | ||
===Anti-histamines=== | ===Anti-histamines=== | ||
* Diphenhydramine | * [[Diphenhydramine]] | ||
===Gamma-aminobutyric acid (GABA) agonists=== | ===Gamma-aminobutyric acid (GABA) agonists=== | ||
Gamma-aminobutyric acid (GABA) the major inhibitory neurotransmitter in the central nervous system.<ref name="isbn0-07-145153-6">{{cite book |author=Katzung, Bertram G. |title=Basic and clinical pharmacology |publisher=McGraw-Hill Medical Publishing Division |location=New York |year=2006 |pages= |isbn=0-07-145153-6 |oclc= |doi=}}</ref> Drugs that increase the effect of GABA are called GABAergic. | [[Gamma-aminobutyric acid]] (GABA) the major inhibitory neurotransmitter in the central nervous system.<ref name="isbn0-07-145153-6">{{cite book |author=Katzung, Bertram G. |title=Basic and clinical pharmacology |publisher=McGraw-Hill Medical Publishing Division |location=New York |year=2006 |pages= |isbn=0-07-145153-6 |oclc= |doi=}}</ref> Drugs that increase the effect of GABA are called GABAergic. | ||
Many sedatives work by increasing receptiveness of GABA<sub>A</sub> receptors. | Many sedatives work by increasing receptiveness of GABA<sub>A</sub> receptors. | ||
====Barbituates==== | ====Barbituates==== | ||
Barbituates are GABAergic by increasing receptiveness of the GABA<sub>A</sub> receptors. Barbituates do this by increasing the duration of openings of channels in the cell membrane.<ref name="isbn0-07-145153-6"/> | [[Barbituates|Barbituates]] are GABAergic by increasing receptiveness of the GABA<sub>A</sub> receptors. Barbituates do this by increasing the duration of openings of channels in the cell membrane.<ref name="isbn0-07-145153-6"/> | ||
* Phenobarbital | * Phenobarbital | ||
| Line 24: | Line 25: | ||
Benzodiazepines are also GABAergic by increasing receptiveness of the GABA<sub>A</sub> receptors. However, benzodiazepines do this by increasing the frequency of openings of channels in the cell membrane.<ref name="isbn0-07-145153-6"/> | Benzodiazepines are also GABAergic by increasing receptiveness of the GABA<sub>A</sub> receptors. However, benzodiazepines do this by increasing the frequency of openings of channels in the cell membrane.<ref name="isbn0-07-145153-6"/> | ||
[[Benzodiazepine]] receptors are BZ<sub>1</sub> and BZ<sub>2</sub>. | |||
=====Non-selective agonists===== | =====Non-selective agonists===== | ||
* Diazepam (Valium) | * [[Diazepam]] ([[Valium]]) | ||
=====BZ<sub>1</sub> selective agonists===== | =====BZ<sub>1</sub> selective agonists===== | ||
* Zaleplon | * [[Zaleplon]] | ||
* Zolpidem | * [[Zolpidem]] | ||
===Serotonin (5-HT) agonists=== | ===Serotonin (5-HT) agonists=== | ||
Agonists of the 5-HT<sub>1A</sub> receptor can cause sedation. | Agonists of the 5-HT<sub>1A</sub> receptor can cause sedation. | ||
* Buspirone | * [[Buspirone]] | ||
==References== | ==References== | ||
<references/> | <references/> | ||
Revision as of 18:44, 29 December 2007
Classification
Below are examples of available sedative drugs.
Alcohols
Ethylene glycols
Anti-adrenergics
Inhibitors of the adrenergic alpha-2 receptor can cause sedation.
- Dexmedetomidine. In some settings, dexmedetomidine may cause less adverse drug reactions than non-selective benzodiazepams.[1]
Anti-histamines
Gamma-aminobutyric acid (GABA) agonists
Gamma-aminobutyric acid (GABA) the major inhibitory neurotransmitter in the central nervous system.[2] Drugs that increase the effect of GABA are called GABAergic.
Many sedatives work by increasing receptiveness of GABAA receptors.
Barbituates
Barbituates are GABAergic by increasing receptiveness of the GABAA receptors. Barbituates do this by increasing the duration of openings of channels in the cell membrane.[2]
- Phenobarbital
Benzodiazepines
Benzodiazepines are also GABAergic by increasing receptiveness of the GABAA receptors. However, benzodiazepines do this by increasing the frequency of openings of channels in the cell membrane.[2]
Benzodiazepine receptors are BZ1 and BZ2.
Non-selective agonists
BZ1 selective agonists
Serotonin (5-HT) agonists
Agonists of the 5-HT1A receptor can cause sedation.
References
- ↑ Pandharipande PP, Pun BT, Herr DL, et al (2007). "Effect of sedation with dexmedetomidine vs lorazepam on acute brain dysfunction in mechanically ventilated patients: the MENDS randomized controlled trial". JAMA 298 (22): 2644–53. DOI:10.1001/jama.298.22.2644. PMID 18073360. Research Blogging.
- ↑ 2.0 2.1 2.2 Katzung, Bertram G. (2006). Basic and clinical pharmacology. New York: McGraw-Hill Medical Publishing Division. ISBN 0-07-145153-6.