ADENOSINE

Q.) Adenosine false are-
a. This has a half-life of approximately 10 min
b. It is a naturally occurring purine nucleoside
c. It is useful in the management of supraventricular and ventricular arrhythmias
d. It is the drug of choice to cardiovert patients with tachycardias related to Wolff–Parkinson–White syndrome

Ans: A, C, D.

Adenosine is a naturally occurring purine nucleoside that has a half-life of approximately 10 seconds, so its side effects, such as dyspnoea and bronchospasm, are short-lived. It is useful in supraventricular tachycardia via its action at the AV (atrioventricular) node. In Wolff–Parkinson–White (WPW) syndrome, adenosine (and other AV node-blocking drugs such as calcium channel blockers, b blockers and digoxin) may cause a faster ventricular rate from unopposed and potentially enhanced conduction through an accessory pathway. This may degenerate in ventricular fibrillation.


ADENOSINE  is a nucleoside that is administered as a rapid intravenous bolus for the acute termination of reentrant supraventricular arrhythmias. Rare cases of ventricular tachycardia ( These may be harmful in reentrant VT and so should be used for acute therapy only if the diagnosis is secure) in patients with otherwise normal hearts are thought to be DAD-mediated and can be terminated by adenosine. Adenosine also has been used to produce controlled hypotension during some surgical procedures and in the diagnosis of coronary artery disease. 
The effects of adenosine are mediated via specific GPCRs. Adenosine activates acetylcholine-sensitive K+ current in the atrium and sinus and AV nodes, resulting in shortening of action potential duration, hyperpolarization, and slowing of normal automaticity. Adenosine also inhibits the electrophysiological effects of increased cellular cyclic AMP that occur with sympathetic stimulation. Because adenosine thereby reduces Ca2+ currents, it can be antiarrhythmic by increasing AV nodal refractoriness and by inhibiting DADs elicited by sympathetic stimulation. Administration of an intravenous bolus of adenosine transiently slows sinus rate and AV nodal conduction velocity and increases AV nodal refractoriness. A bolus of adenosine can produce transient sympathetic activation by interacting with carotid baroreceptors; a continuous infusion can cause hypotension. 
 Adverse Effects : A major advantage of adenosine therapy is that adverse effects are short-lived because the drug is transported into cells and deaminated so rapidly. Transient asystole is common but usually lasts less than 5 seconds and is in fact the therapeutic goal. Most patients feel a sense of chest fullness and dyspnea when therapeutic doses (6–12 mg) of adenosine are administered. Rarely, an adenosine bolus can precipitate bronchospasm or atrial fibrillation.
Clinical Pharmacokinetics:  Adenosine is eliminated with a t1/2 of 10 seconds by carrier-mediated uptake in most cell types and subsequent metabolism by adenosine deaminase. Adenosine probably is the only antiarrhythmic drug whose efficacy requires a rapid bolus dose, preferably through a large central intravenous line; slow administration permits elimination of the drug prior to its arrival at the heart. The effects of adenosine are potentiated in patients receiving dipyridamole, an adenosine-uptake inhibitor, and in patients with cardiac transplants owing to denervation hypersensitivity. Methylxanthines (e.g., theophylline and caffeine) block adenosine receptors; therefore, larger than usual doses are required to produce an antiarrhythmic effect in patients who have consumed these agents in beverages or as therapy. 


source: Goodman Gilman textbook of pharmacology