TY - JOUR
T1 - Effects of adrenaline on electrophysiological parameters during short exposure to global ischemia. A ventricular fibrillation study in isolated heart
AU - Amitzur, Giora
AU - Shenkar, Nitza
AU - Leor, Jonathan
AU - Novikov, Ilia
AU - Eldar, Michael
N1 - Funding Information:
This study was supported by a grant from the Ministry of Science, project No. DISMED 0091/GR 01368. We wish to thank Mr. Eli Zimmerman for his assistance in constructing part of the equipment and Mrs. Elaine Finkelstein and Vivienne York for their help in editing the manuscript.
PY - 2002
Y1 - 2002
N2 - Background. The mechanisms by which adrenaline may enhance defibrillation success rate, is poorly understood. Objectives. To study electrophysiological effects of adrenaline during short exposure to global ischemia. Methods. In isolated perfused feline hearts, coronary perfusion was eliminated repeatedly for 1 min with 10 rain reperfusion intervals. Treatment included: (1) continuous perfusion alone - Control, (2) global ischemia alone, (3) adrenaline (10-7 M) during perfusion, (4) adrenaline (10-7 M) during global ischemia (n = 10), in separate hearts, (5) control and higher adrenaline concentration (1 × 10-6 M), (6) during perfusion, (7) during global ischemia (n = 9). Measurements during pacing included: (1) diastolic threshold of excitability; (2) refractoriness; (3) epicardial conduction time; and (4) all tissue resistivity to indirectly detect changes in passive properties of conduction. Measurements during 1 min (or 90 sec) of electrically induced ventricular fibrillation included - All tissue resistivity and, based on maximal entropy spectral analysis and normalized entropy, rate of arrhythmia and degree of arrhythmia organization. Results. Adrenaline (10-7 M) during global ischemia vs control caused spontaneous arrhythmia termination, increased threshold significantly but reduced conduction time. Higher adrenaline concentration (1 × 10-6 M) during global ischemia improved the passive properties of conduction and arrhythmia organization and reduced arrhythmia rate. Global ischemia alone increased conduction time but had a deleterious effect on passive properties. Adrenaline (10-7 M) during perfusion improved conduction, but did so less than during global ischemia. Higher adrenaline concentration during perfusion (10-6 M) improved arrhythmia organization and caused spontaneous arrhythmia termination but again less than during global ischemia. Conclusions. During short periods of global ischemia adrenaline improved the passive properties of conduction and arrhythmia organization, reduced arrhythmia rate and increased its spontaneous termination. Such changes may be operative in improving defibrillation success.
AB - Background. The mechanisms by which adrenaline may enhance defibrillation success rate, is poorly understood. Objectives. To study electrophysiological effects of adrenaline during short exposure to global ischemia. Methods. In isolated perfused feline hearts, coronary perfusion was eliminated repeatedly for 1 min with 10 rain reperfusion intervals. Treatment included: (1) continuous perfusion alone - Control, (2) global ischemia alone, (3) adrenaline (10-7 M) during perfusion, (4) adrenaline (10-7 M) during global ischemia (n = 10), in separate hearts, (5) control and higher adrenaline concentration (1 × 10-6 M), (6) during perfusion, (7) during global ischemia (n = 9). Measurements during pacing included: (1) diastolic threshold of excitability; (2) refractoriness; (3) epicardial conduction time; and (4) all tissue resistivity to indirectly detect changes in passive properties of conduction. Measurements during 1 min (or 90 sec) of electrically induced ventricular fibrillation included - All tissue resistivity and, based on maximal entropy spectral analysis and normalized entropy, rate of arrhythmia and degree of arrhythmia organization. Results. Adrenaline (10-7 M) during global ischemia vs control caused spontaneous arrhythmia termination, increased threshold significantly but reduced conduction time. Higher adrenaline concentration (1 × 10-6 M) during global ischemia improved the passive properties of conduction and arrhythmia organization and reduced arrhythmia rate. Global ischemia alone increased conduction time but had a deleterious effect on passive properties. Adrenaline (10-7 M) during perfusion improved conduction, but did so less than during global ischemia. Higher adrenaline concentration during perfusion (10-6 M) improved arrhythmia organization and caused spontaneous arrhythmia termination but again less than during global ischemia. Conclusions. During short periods of global ischemia adrenaline improved the passive properties of conduction and arrhythmia organization, reduced arrhythmia rate and increased its spontaneous termination. Such changes may be operative in improving defibrillation success.
KW - Adrenergic agonists
KW - Cell communication
KW - Conduction
KW - Defibrillation
KW - Global ischemia
KW - Ventricular fibrillation
UR - http://www.scopus.com/inward/record.url?scp=0035997527&partnerID=8YFLogxK
U2 - 10.1023/A:1015749331517
DO - 10.1023/A:1015749331517
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AN - SCOPUS:0035997527
SN - 0920-3206
VL - 16
SP - 111
EP - 119
JO - Cardiovascular Drugs and Therapy
JF - Cardiovascular Drugs and Therapy
IS - 2
M1 - 5087874
ER -