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| __NOTOC__
| | #REDIRECT [[Adenosine#Pharmacology]] |
| {{Adenosine}}
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| {{CMG}}; {{AE}} {{AZ}}
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| ==Clinical Pharmacology==
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| ===Mechanism of Action===
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| Adenocard (adenosine injection) slows conduction time through the A-V node, can interrupt the reentry pathways through the [[A-V node]], and can restore normal sinus rhythm in patients with [[paroxysmal supraventricular tachycardia]] (PSVT), including PSVT associated with [[Wolff-Parkinson-White Syndrome]].
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| Adenocard is antagonized competitively by methylxanthines such as caffeine and [[theophylline]], and potentiated by blockers of nucleoside transport such as dipyridamole. Adenocard is not blocked by [[atropine]].
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| ===Hemodynamics===
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| The intravenous bolus dose of 6 or 12 mg Adenocard (adenosine injection) usually has no systemic hemodynamic effects. When larger doses are given by infusion, adenosine decreases blood pressure by decreasing peripheral resistance.
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| ===Pharmacokinetics===
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| Intravenously administered adenosine is rapidly cleared from the circulation via cellular uptake, primarily by erythrocytes and vascular endothelial cells. This process involves a specific transmembrane nucleoside carrier system that is reversible, nonconcentrative, and bidirectionally symmetrical. Intracellular adenosine is rapidly metabolized either via phosphorylation to adenosine monophosphate by adenosine kinase, or via deamination to inosine by adenosine deaminase in the cytosol. Since adenosine kinase has a lower Km and Vmax than adenosine deaminase, deamination plays a significant role only when cytosolic adenosine saturates the phosphorylation pathway. Inosine formed by deamination of adenosine can leave the cell intact or can be degraded to hypoxanthine, xanthine, and ultimately uric acid. Adenosine monophosphate formed by phosphorylation of adenosine is incorporated into the high-energy phosphate pool. While extracellular adenosine is primarily cleared by cellular uptake with a half-life of less than 10 seconds in whole blood, excessive amounts may be deaminated by an ecto-form of adenosine deaminase. As Adenocard requires no hepatic or renal function for its activation or inactivation, hepatic and renal failure would not be expected to alter its effectiveness or tolerability.<ref name="dailymed.nlm.nih.gov">{{Cite web | last = | first = | title = ADENOCARD (ADENOSINE) SOLUTION [ASTELLAS PHARMA US, INC.] | url = http://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=f0e32589-dad9-4887-8481-bcf7f6618466 | publisher = | date = | accessdate = }}</ref>
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| ==References==
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| {{Reflist}}
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| {{FDA}}
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| [[Category:Drugs]]
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| {{Reflist|2}}
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| [[Category:Drugs]]
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| [[Category:Antiarrhythmic agents]]
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