D Boros, et. al.
It is clinically established that adenosine has negative chronotropic, antiarrhythmic effects and reduces arterial blood pressure. Adenosine addition to cardioplegic solutions used in cardiac operations is clinically well tolerated and has been shown to improve myocardial protection in several studies. However, the mechanism of action remains unclear. Therefore, it is important to define the effect of adenosine on the inflammatory cascade as immune cell activation occurs early during ischemia reperfusion injury. Adenosine appears to mediate the initial steps of the inflammatory cascade via its four G-coupled protein receptors: A1, A2A, A2B, and A3, expressed on neutrophils, lymphocytes and macrophages. The adenosine receptor isotype dictates the immune response. More specifically, the A1 and A3 receptors stimulate a pro-inflammatory immune response whereas the A2A and A2B are immunosuppressive. As the adenosine receptors are important for cardiac pre-conditioning and post-conditioning, adenosine may regulate the inflammatory responses initiated during ischemia-mediated immune injury related to myocardial protection.
Nikhil Kapoor, et. al.
Despite the use of embolic protection devices, no-reflow can still occur during saphenous vein grafts (SVGs) intervention. High-dose intracoronary adenosine infusion preconditions the myocardium, improves coronary flow, and prevents no-reflow. The role of high-dose intragraft adenosine infusion on protection of microvascular function and prevention of no-reflow has not been investigated. Our aim is to investigated the cardioprotective effect of high-dose intragraft adenosine infusion, compared with placebo, on microvascular function and prevention of no-reflow during SVGs intervention.
This study provides the first evidence that high-dose intragraft adenosine infusion compared with placebo protects microvascular function and prevents no-reflow during SVGs intervention.
L Cheng, et. al.
Paroxysmal supraventricular tachycardia (PSVT) is one of the more common arrhythmias requiring treatment in the emergency department. Intravenous adenosine is recommended as the initial medication of choice for treatment of PSVT, given in escalating doses up to a maximum of 12 mg. In over 10% of adult patients, PSVT will not be terminated with maximum doses of adenosine. We report a case of a patient requiring a higher-than recommended dose of adenosine for termination of PSVT. The patient had a history of pulmonary hypertension with resultant right heart failure at the time of presentation. We believe the higher dose of adenosine was necessary in this patient because of the impaired venous return to her right heart. This case indicates that patients with impaired venous return to the right heart may require higher-than-recommended doses of adenosine for effective termination of PSVT.
M Zehender, et. al.
Adenosine is an endogenous nucleoside which causes a brief blockade of the AV nodal conduction pathway following intravenous administration. Such a brief AV block can be used therapeutically for reliable termination of AV nodal re-entry tachycardia and WPW re-entry tachycardia. It can also be used for demasking atrial activity in rapid suspected supraventricular tachycardia with a broad QRS complex or a Delta wave, not present during sinus rhythm with normal AV node conduction, indicating the presence of a hidden WPW syndrome. Side effects after adenosine application are frequent, but very transient rarely serious (1-3% of cases, e.g. status asthmaticus, ventricular fibrillation) and therefore require a certain degree of experience with this drug on the part of the treating physician.
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