Amitzur Giora, Shenkar Nitza, Leor Jonathan, Novikov Ilia, Eldar Michael
Neufeld Cardiac Research Institute, Tel-Aviv University, Tel-Hashomer, Israel.
Cardiovasc Drugs Ther. 2002 Mar;16(2):111-9. doi: 10.1023/a:1015749331517.
The mechanisms by which adrenaline may enhance defibrillation success rate, is poorly understood.
To study electrophysiological effects of adrenaline during short exposure to global ischemia.
In isolated perfused feline hearts, coronary perfusion was eliminated repeatedly for 1 min with 10 min 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 x 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.
Adrenaline (10(-7) M) during global ischemia vs control caused spontaneous arrhythmia termination, increased threshold significantly but reduced conduction time. Higher adrenaline concentration (1 x 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.
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.
肾上腺素提高除颤成功率的机制尚不清楚。
研究短暂全心缺血期间肾上腺素的电生理效应。
在离体灌注猫心脏中,冠状动脉灌注反复中断1分钟,再灌注间隔为10分钟。处理包括:(1)单纯持续灌注——对照,(2)单纯全心缺血,(3)灌注期间给予肾上腺素(10⁻⁷M),(4)全心缺血期间给予肾上腺素(10⁻⁷M)(n = 10),每组使用不同心脏,(5)对照及更高浓度肾上腺素(1×10⁻⁶M),(6)灌注期间,(7)全心缺血期间(n = 9)。起搏期间的测量指标包括:(1)舒张期兴奋性阈值;(2)不应期;(3)心外膜传导时间;(4)所有组织电阻抗,以间接检测传导的被动特性变化。电诱发心室颤动1分钟(或90秒)期间的测量指标包括——所有组织电阻抗,以及基于最大熵谱分析和标准化熵的心律失常发生率和心律失常组织程度。
全心缺血期间给予肾上腺素(10⁻⁷M)与对照相比,可使自发性心律失常终止,阈值显著升高但传导时间缩短。全心缺血期间更高浓度肾上腺素(1×10⁻⁶M)改善了传导的被动特性和心律失常组织程度,并降低了心律失常发生率。单纯全心缺血增加了传导时间,但对被动特性有有害影响。灌注期间给予肾上腺素(10⁻⁷M)改善了传导,但效果不如全心缺血期间。灌注期间更高浓度肾上腺素(10⁻⁶M)改善了心律失常组织程度并导致自发性心律失常终止,但同样不如全心缺血期间效果明显。
在短暂全心缺血期间,肾上腺素改善了传导的被动特性和心律失常组织程度,降低了心律失常发生率并增加了其自发性终止。这些变化可能有助于提高除颤成功率。