1. Mechanisms of Adenosine-Mediated Actions on Cellular and Clinical Cardiac Electrophysiology 
Win-Kuang Shen, M.D., Yoshihisa Kurachi, M.D., PH.D. 
Mayo Clinic Proceedings 
Volume 70, Issue 3, Pages (March 1995)
DOI: /
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2. Fig. 1
Adenosine metabolism. ADP = adenosine diphosphate; AMP =adenosine monophosphate; ATP =adenosine triphosphate; SAH =S-adenosyl homocystine.
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3. Fig. 2
Conductance and kinetic properties of adenosine- and acetylcholine-regulated channel activity. A, Adenosine (Ado)- and acetylcholine (ACh)-regulated channel currents recorded from guinea pig atrial myocytes at various membrane potentials in cell-attached patch-clamp configuration. Pipettes contained Ado (10 μM) or ACh (5.5/μM). All records were low-pass filtered at 1 kHz (-3 dB). Arrowhead (each trace) = zero current level. B, Current-voltage relationships of Ado-(closed circles) and ACh (open circles)-regulated channels. In this example, slope conductance of unitary current was 46 pS. C, Open time histograms of Ado- and ACh-regulated channels at Er. Both distributions were fitted by single exponential curve with time constant indicated in each graph. (From Kurachi and associates.39 By permission.)
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4. Fig. 3
Scheme of purinergic and muscarinic activation of K channel in atrial cell membrane. In cardiac atrial cell membrane, two membrane receptors (P1-purinergic and muscarinic [M] acetylcholine [ACh] receptors) are linked to Kchannel through guanosine triphosphate (GTP)-binding proteins (GK). Quantitative relationships between components are not represented in scheme. Ado = adenosine; GDP = guanosine diphosphate; Pi = phosphate. (Modified from Kurachi and associates.39 By permission.)
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5. Fig. 4
Scheme of activation of K+ channel regulated by guanosine triphosphate (GTP)-binding protein in atrial cell membrane. A = agonist (acetylcholine or adenosine); α, β, and γ= subunits of GTP-binding protein; GDP = guanosine diphosphate; Pi = phosphate; R = membrane receptor (muscarinic or A1 receptor). Scheme does not represent any quantitative relationships and does not exclude possibility of several states other than 1,2, and 3, as shown. (Modified from Kurachi and associates.42 By permission.)
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6. Fig. 5
Proposed mechanism for pertussis toxin-sensitive G-protein subunit activation of potassium adenosine triphosphate (KATP) and potassium acetylcholine (KAch) channelsin cardiaccell membrane. After stimulation of receptors (R) by adenosine or acetylcholine (ACh), pertussis toxin-sensitive G proteins may be functionally dissociated into Gα-guanosine triphosphate (GTP) and Gβγ. Gα-GTP maya ctivate KATP channel, and Gβγ mayactivate KAch channel. Former mechanism exists in both ventricular and atrial cells, and latter may exist in atrial but not in ventricular cells. Scheme does not represent any quantitative relationship between each component and does not considerall possible intermediate steps between components. α, β, and γ = subunits of GTP-binding protein. (Modified from ito and associates.52 Bypermission.)
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7. Fig. 6
Signal transduction mechanisms responsible for direct and indirect effects of adenosine in cardiac myocytes. A1 = adenosine receptor; AC = adenylate cyclase; AMP = adenosine monophosphate; ATP =adenosine triphosphate; β1 =adrenergic receptor; cAMP =cyclic AMP; cGMP =cyclic guanosine monophosphate; Gi=inhibitory G protein; GK = guanosine triphosphate-binding proteins; Gs = stimulatory G protein; KACh =potassium acetylcholine; M2 =muscarinic receptor; PDE =phosphodiesterase; PKA =protein kinase A; PO4 =phosphorylation; R =receptor.
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8. Fig. 7
Effects of adenosine (15 s after intravenous injection) on atrioventricular nodal conduction. Top two tracings are from surface electrocardiogram leads I and V1. All numbers are in milliseconds. A-H = upper atrioventricular junction conduction time including atrioventricular node; HBE = His-bundle electrogram; H-V = His bundle to ventricular conduction; HRA = high right atrial intracardiac recording; RV = right ventricular intracardiac recording.
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9. Fig. 8
A, Twelve-lead electrocardiogram, showing narrow complex tachycardia at rate of about 200 beats/min, B, During electrophysiologic testing, narrow complex tachycardia was induced during atrial-programmed stimulation consistent with atrioventricular (AV) nodal reentrant tachycardia and terminated by injection of 6 mg of adenosine. Top two tracings are from surface electrocardiogram leads I and V1. AV nodal reentry tachycardia was terminated with retrograde atrial recording (fast pathway conduction) and blocked in slow pathway in anterograde direction above His bundle, First QRS complex after termination of tachycardia is fusion beat. After injection of adenosine, premature ventricular contractions are common (see text for discussion). Presence of accessory pathway was excluded during electrophysiologic testing, HBE = intracardiac His-bundle electrogram; HRA = high right atrium intracardiac recording; RVA = intracardiac recording from right ventricular apex.
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10. Fig. 9
A, Base 12-lead electrocardiogram, showing preexcitation consistent with diagnosis of Wolff-Parkinson-White syndrome. B, Twelve-lead electrocardiogram, showing narrow complex tachycardia consistent with orthodromic atrioventricular tachycardia. C, Recordings from electrophysiologic testing; top two tracings are from surface electrocardiogram leads I and V1. Activation sequence during tachycardia is consistent with left-sided accessory pathway. Adenosine terminated tachycardia (atrial recording). Block occurred at atrioventricular node above His bundle (absence of His-bundle signal). DCS, MCS, and PCS = recordings from distal, mid, and proximal coronary sinus electrodes, respectively. HBE =His-bundle recording; HRA =intracardiac recording from high right atrium; RVA = right ventricular apex recording.
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11. Fig. 10
Responseof ectopic atrial tachycardia(automatic) to adenosine. Recordings are from surface electrocardiogram leads I, II, and III. A, P-wavemorphology in leads II and III suggestsatrial ectopic focus (inverted P wave). After 12mg of adenosine was administered, ectopic focus was transiently suppressed, and sinus node activitywas apparent(upright P wave). B, Effect of adenosine was transient, as shown by return of ectopic focus shortly after adenosine injection
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12. Fig. 11
A, Twelve-lead electrocardiogram of young man with wide complex tachycardia, which began during basketball game. Typically, this tachycardia has left bundle branch block morphology with inferior axis. B, Single-lead electrocardiogram, showing tachycardia was terminated after intravenous injection of adenosine (6 mg). This tachycardia was subsequently induced during electrophysiologic testing with isoproterenol challenge(3 μg/min),
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13. Fig. 12
Use of adenosine in diagnosis of and therapy for tachyarrhythmias (see text for discussion). AFiblWPW = atrial fibrillation/Wolff-Parkinson-White syndrome; AT = atrial tachycardia; AVNRT = atrioventricular nodal reentrant tachycardia; AVRT = atrioventricular reentrant tachycardia; ECG = electrocardiographic; Hx =history; la drugs = disopyramide, procainamide, and quinidine; Ic drugs = propafenone and flecainide; RVOT =right ventricular outflow tract; SNRT = sinus node reentrant tachycardia; SVT =supraventricular tachycardia; VT = ventricular tachycardia;* =transient suppression.
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14. Fig. 13
Twelve-lead electrocardiogram (A) showing atrial fibrillation with preexcitation (Wolff-Parkinson-White syndrome). Ventricular rate was increased substantially after 6 mg (B) and 12 mg (C) of adenosine was injected intravenously.
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