Alpha-Monoacetyldigitoxin
Alpha-Monoacetyldigitoxin Uses, Dosage, Side Effects, Food Interaction and all others data.
Cardioactive derivative of lanatoside A or of digitoxin used for fast digitalization in congestive heart failure.
The main pharmacological effects of acetyldigitoxin are on the heart. Extracardiac effects are responsible for many of the adverse effects. Its main cardiac effects are 1) a decrease of conduction of electrical impulses through the AV node, making it a commonly used drug in controlling the heart rate during atrial fibrillation or atrial flutter, and 2) an increase of force of contraction via inhibition of the Na+/K+ ATPase pump.
Trade Name | Alpha-Monoacetyldigitoxin |
Generic | Acetyldigitoxin |
Acetyldigitoxin Other Names | Acetildigitoxina, Acetyl-digitoxin-alpha, Acetyldiginatin, Acetyldigitoxin, Acetyldigitoxinum, Acetylgitoxin, alpha-Acetyldigitoxin, alpha-Acetylgitaloxin, alpha-Monoacetyldigitoxin, Desglucolanatoside A, Digitoxin 3'''-acetate |
Type | |
Formula | C43H66O14 |
Weight | Average: 806.9757 Monoisotopic: 806.44525682 |
Groups | Approved |
Therapeutic Class | |
Manufacturer | |
Available Country | |
Last Updated: | September 19, 2023 at 7:00 am |
Uses
Used for fast digitalization in congestive heart failure.
How Alpha-Monoacetyldigitoxin works
Alpha-Monoacetyldigitoxin binds to a site on the extracellular aspect of the α-subunit of the Na+/K+ ATPase pump in the membranes of heart cells (myocytes). This causes an increase in the level of sodium ions in the myocytes, which then leads to a rise in the level of calcium ions. The proposed mechanism is the following: inhibition of the Na+/K+ pump leads to increased Na+ levels, which in turn slows down the extrusion of Ca2+ via the Na+/Ca2+ exchange pump. Increased amounts of Ca2+ are then stored in the sarcoplasmic reticulum and released by each action potential, which is unchanged by acetyldigitoxin. This is a different mechanism from that of catecholamines. Alpha-Monoacetyldigitoxin also increases vagal activity via its central action on the central nervous system, thus decreasing the conduction of electrical impulses through the AV node. This is important for its clinical use in different arrhythmias.
Toxicity
Toxicity includes ventricular tachycardia or ventricular fibrillation, or progressive bradyarrhythmias, or heart block. LD50 = 7.8 mg/kg (orally in mice).
Elimination Route
Bioavailability is 60 to 80% following oral administration.
Innovators Monograph
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