WordNet

the 3rd letter of the Roman alphabet (同)c
(music) the keynote of the scale of C major
a general-purpose programing language closely associated with the UNIX operating system
capable of depressing physiological or psychological activity or response by a chemical agent

PrepTutorEJDIC

carbonの化学記号
機能低下剤,鎮静剤,抑制剤 / 鎮静効果のある / 意気消沈させる / 物価を抑制する

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2016/02/10 11:55:05」(JST)

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Central nervous system depression or CNS depression refers to physiological depression of the central nervous system that can result in decreased rate of breathing, decreased heart rate, and loss of consciousness possibly leading to coma or death. CNS depression is specifically the result of inhibited brain activity.^[1]

Causes

CNS depression is generally caused by the use of depressant drugs such as alcohol, opioids, barbiturates, benzodiazepines, general anesthetics, and anticonvulsants such as pregabalin used to treat epilepsy. ^[2] ^[3] Drug overdose is often caused by combining two or more depressant drugs, although overdose is certainly possible by consuming a large dose of one depressant drug. CNS depression can also be caused by the accidental or intentional inhalation or ingestion of certain volatile chemicals such as Butanone (contained in Plastic Cement) or Isopropyl Alcohol. Other causes of CNS depression are metabolic disturbances such as hypoglycaemia.^{[citation needed]}

Comparison

In a study comparing the central nervous depression due to supra-therapeutic doses of Triazolam (Benzodiazepine), Pentobarbital (Barbiturate) and GHB it appeared as if GHB had the strongest dose-effect function. Since, GHB had a high correlation between its dose and its central nervous system depression it has a high risk of accidental overdose. In the case of accidental overdose of GHB, patients could become drowsy, fall asleep and may enter a coma. Although GHB had higher sedative effects at high doses as compared to Triazolam and Pentobarbital, it had less amnestic effects as compared to Triazolam and Pentobarbital. Arousal of subjects in the GHB group sometimes even required a painful stimulus, this was not seen in the Triazolam or the Pentobarbital group. Fortunately, during this heavy sedation with GHB the subjects maintained normal respiration and blood pressure. This is often not the case with opioids as they will cause respiratory depression.^[4]

Treatment

CNS depression is treated within a hospital setting by maintaining breathing and circulation. Individuals with reduced breathing may be given supplemental oxygen, while individuals who are not breathing can be ventilated with bag valve mask ventilation or by mechanical ventilation with a respirator. Sympathomimetic drugs may be used to attempt to stimulate cardiac output in order to maintain circulation. CNS Depression caused by certain drugs may respond to treatment with an antidote.^{[citation needed]}

There are two antidotes that are frequently used in the hospital setting and these are Naloxone and Flumazenil. Naloxone is an opioid antagonist and reverses the central nervous depressive effects seen in opioid overdose. In the setting of a colonoscopy, Naloxone is rarely administered but when it is administered, its half life is shorter than some common opioid agonists. Therefore the patient may still exhibit central nervous system depression after Naloxone has been cleared. Typically, Naloxone is administered in short intervals with relatively small doses in order to prevent the occurrence of withdrawal, pain, and sympathetic nervous system activation. Flumazenil is a benzodiazepine antagonists and blocks the binding of benzodiazepines to GABAa. Similarly to Naloxone, Flumazenil has a short half life, and this needs to be taken into account because the patient may exhibit central nervous depression after the antidote has been cleared. Benzodiazepines are used in the treatment of seizures and subsequently, the administration of Flumazenil may result in seizures. Therefore, slow administration of Flumazenil is necessary to prevent the occurrence of a seizure. These agents are rarely used in the setting of a colonoscopy as 98.8% of colonoscopies use sedatives but only 0.8% of them result in the administration of one of these antidotes. Even if they are rarely used in colonoscopies they are important in preventing the patient from entering a coma or developing respiratory depression when sedatives are not properly dosed. Outside of the colonoscopy setting, these agents are used for other procedures and in the case of drug overdose.^[5]

References

^ "How do CNS depressants affect the brain and body?". National Institute of Health. October 2011.
^ "What are CNS depressants?". National Institute of Health. October 2011.
^ Adam Cloe (Jun 30, 2010). "What Is CNS Depression?". www.livestrong.com.
^ http://www.nature.com/npp/journal/v31/n11/full/1301146a.html
^ http://www.karger.com/Article/FullText/285519

UpToDate Contents

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1. 慢性疼痛の治療の概要 overview of the treatment of chronic pain
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3. 高齢者における単極性うつ病の診断およびマネージメント diagnosis and management of late life unipolar depression
4. うつ病のスクリーニング screening for depression
5. 成人におけるうつ病：ニューロモデュレーション治療の概要 depression in adults overview of neuromodulation procedures

English Journal

A Multifaceted GABAA Receptor Modulator: Functional Properties and Mechanism of Action of the Sedative-Hypnotic and Recreational Drug Methaqualone (Quaalude).

Hammer H1, Bader BM1, Ehnert C1, Bundgaard C1, Bunch L1, Hoestgaard-Jensen K1, Schroeder OH1, Bastlund JF1, Gramowski-Voß A1, Jensen AA2.
Molecular pharmacology.Mol Pharmacol.2015 Aug;88(2):401-20. doi: 10.1124/mol.115.099291. Epub 2015 Jun 8.
In the present study, we have elucidated the functional characteristics and mechanism of action of methaqualone (2-methyl-3-o-tolyl-4(3H)-quinazolinone, Quaalude), an infamous sedative-hypnotic and recreational drug from the 1960s-1970s. Methaqualone was demonstrated to be a positive allosteric modu
PMID 26056160

Enhancement of endocannabinoid signaling protects against cocaine-induced neurotoxicity.

Vilela LR1, Gobira PH2, Viana TG2, Medeiros DC3, Ferreira-Vieira TH3, Doria JG1, Rodrigues F4, Aguiar DC2, Pereira GS3, Massessini AR3, Ribeiro FM4, de Oliveira AC2, Moraes MF5, Moreira FA6.
Toxicology and applied pharmacology.Toxicol Appl Pharmacol.2015 Aug 1;286(3):178-87. doi: 10.1016/j.taap.2015.04.013. Epub 2015 Apr 29.
Cocaine is an addictive substance with a potential to cause deleterious effects in the brain. The strategies for treating its neurotoxicity, however, are limited. Evidence suggests that the endocannabinoid system exerts neuroprotective functions against various stimuli. Thus, we hypothesized that in
PMID 25933444

Potential Adverse Effects of Anesthesia in Children--Reply.

Psaty BM1, Platt R2, Altman RB3.
JAMA.JAMA.2015 Jul 28;314(4):409. doi: 10.1001/jama.2015.7387.
PMID 26219066

Japanese Journal

Histidine-Related Dipeptides, Carnosine, Anserine and Homocarnosine, Possess the CNS Depressant Effects on Mice and their Action Mechanism

USAMI Noriyuki,KISHI Nobuyuki,IKEBE Katsuhiko,KUBOTA Yu-ki,FUKUSHIMA Tomonori,KIMURA Toshiyuki,YAMAMOTO Ikuo
Peptide science : proceedings of the ... Japanese Peptide Symposium 2010, 86, 2011-03-01
NAID 10028237355

Sedative and anxiolytic effects of the methanolic extract of Leea indica (Burm. f.) Merr. leaf

, , , , ,
Drug Discoveries & Therapeutics 5(4), 185-189, 2011
… indica leaves was evaluated for its central nervous system (CNS) depressant effect using rodent behavioral models, such as hole cross, open field and thiopental sodium induced sleeping time tests for its sedative properties and an elevated plus-maze (EPM) test for its anxiolytic potential, respectively. … the highest CNS depressant effect was shown at a dose of 400 mg/kg, p.o. …
NAID 130005054714