 | |
 | |
| Clinical data | |
|---|---|
| MedlinePlus | a682861 |
| Pregnancy category |
|
| Routes of administration | IV,IM |
| ATC code | |
| Legal status | |
| Legal status | |
| Pharmacokinetic data | |
| Bioavailability | NA |
| Protein binding | NA |
| Metabolism | None |
| Eliminationhalf-life | 7-8 hours |
| Excretion | Renal |
| Identifiers | |
| |
| CAS Number |
|
| PubChemCID | |
| IUPHAR/BPS | |
| DrugBank |
|
| ChemSpider |
|
| UNII | |
| KEGG |
|
| ChEBI | |
| ChEMBL | |
| CompTox Dashboard(EPA) | |
| Chemical and physical data | |
| Formula | C11H17BrN+ |
| Molar mass | 243.168 g·mol−1 |
| 3D model (JSmol) | |
| |
| |
 N Y (what is this?) (verify) | |
Bretylium (alsobretylium tosylate) is anantiarrhythmic agent.[1] It blocks the release ofnoradrenaline from nerve terminals. In effect, it decreases output from the peripheralsympathetic nervous system. It also acts by blocking K+ channels and is considered a class III antiarrhythmic. The dose is 5–10 mg/kg and side effects arehigh blood pressure followed bylow blood pressure andventricular ectopy.
Originally introduced in 1959 for the treatment of hypertension.[2] Its use as an antiarrhythmic forventricular fibrillation was discovered and patented by Marvin Bacaner in 1969 at theUniversity of Minnesota.[3]
TheAmerican Heart Association removed bretylium from their 2000 ECC/ACC guidelines due to its unproven efficacy and ongoing supply problems. Many have cited these supply problems as an issue of raw materials needed in the production of Bretylium. By the release of the AHA 2005 ECC/ACC guidelines there is no mention of Bretylium and it is virtually unavailable throughout most of the world.[4][5]
On June 8, 2011 bretyliumtosylate was announced as unavailable in the US after request ofHospira Inc. to withdraw itsNDA from the market. Bretylium will remain on theFDA's discontinued drug list since its withdrawal was not the result of a safety or effectiveness concern.[6] In mid 2019, it was reintroduced.[citation needed]
The drug was used inemergency medicine,cardiology, and other specialties throughout the 1980s-1990s for the acute management ofventricular tachycardia andventricular fibrillation refractory to other first line treatments such as defibrillation or lidocaine.[7]
It is contraindicated in patients withAV (atrioventricular)heart block ordigoxintoxicity.
Bretylium should be used only in anICU or emergency department setting and should not be used elsewhere due to its dramatic actions and its predominant side effect ofhypotension.[citation needed]
It is used in physiological and pharmacological research as an inhibitor of sympathetic transmission. Its mechanism of action is the inhibition of neurotransmitter release from sympathetic nerve terminals, both by the inhibition of action potentials in the nerve terminals and by other mechanisms.[8] Its specificity for sympathetic nerves is achieved because it is a substrate for the noradrenaline transporter;[9] hence, it accumulates inside nerve terminals which have this transporter.
