Deslanoside
(Redirected from Cedilanid-d)
Deslanoside[edit | edit source]
Deslanoside is a cardiac glycoside used in the treatment of certain heart conditions. It is derived from the leaves of the Digitalis lanata plant, commonly known as woolly foxglove. Deslanoside is part of a group of medications that are used to improve the strength and efficiency of the heart, or to control the rate and rhythm of the heartbeat.
Pharmacology[edit | edit source]
Deslanoside works by inhibiting the sodium-potassium ATPase pump, which leads to an increase in intracellular sodium. This increase in sodium promotes the influx of calcium into the heart muscle cells, enhancing cardiac contractility. The increased calcium availability in the heart muscle cells results in a more forceful contraction of the heart, which is beneficial in conditions such as heart failure and atrial fibrillation.
Clinical Use[edit | edit source]
Deslanoside is primarily used in the management of heart failure and certain types of arrhythmias, particularly atrial fibrillation and atrial flutter. It helps to control the heart rate and improve cardiac output, which can alleviate symptoms such as shortness of breath and fatigue in patients with heart failure.
Administration[edit | edit source]
Deslanoside is typically administered intravenously, especially in acute settings where rapid onset of action is required. The dosage of deslanoside must be carefully monitored, as the therapeutic window is narrow and the risk of toxicity is significant.
Side Effects[edit | edit source]
Common side effects of deslanoside include nausea, vomiting, diarrhea, and dizziness. More serious side effects can occur, such as digitalis toxicity, which may present with symptoms like confusion, irregular heartbeats, and visual disturbances. Monitoring of blood levels and renal function is important to prevent toxicity.
Mechanism of Action[edit | edit source]
Deslanoside exerts its effects by binding to and inhibiting the sodium-potassium ATPase pump on the cardiac cell membrane. This inhibition leads to an increase in intracellular sodium levels, which in turn affects the sodium-calcium exchanger, resulting in increased intracellular calcium. The elevated calcium levels enhance the contractile force of the heart muscle, improving cardiac output.
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