Lawson C S, Hearse D J
Wessex Cardiac Unit, Southampton General Hospital, UK.
Cardiovasc Res. 1996 Apr;31(4):655-62.
The present study addresses whether the mechanism of anti-arrhythmic protection by ischaemic preconditioning involves depletion of myocardial catecholamines.
In a randomised series of studies isolated rat hearts, perfused with whole blood, underwent episodes of regional ischaemia and reperfusion induced with a snare around the left coronary artery. Control hearts (Group 1, n = 12) were subjected to 40 min aerobic perfusion, 30 min ischaemia and 10 min reperfusion. Preconditioned hearts (Group 2, n = 12) were subjected to 10 min aerobic perfusion, three cycles of ischaemia and reperfusion (5 min each), 30 min ischaemia and 10 min reperfusion. Cardiac rhythm was recorded continuously and arrhythmias quantified during the final periods of ischaemia and reperfusion. At the end of the experiment samples of right ventricular (RV; non-ischaemic) and left ventricular (LV; ischaemic territory) tissue were separated and frozen. In 5 additional groups (n = 6/group) tissue samples were taken after 10 min aerobic perfusion, after 10 min aerobic perfusion followed by 1, 2 or 3 preconditioning cycles and after 40 min of aerobic perfusion. All tissue samples were analysed for catecholamine content.
Preconditioning resulted in reductions in the incidence of ischaemia-induced VF from 67% in Group 1 to 8% in Group 2, the incidence of ischaemia-induced VT from 100% to 17% and the number of ischaemia-induced VPBs from 246 +/- 25 to 59 +/- 19 (each P < 0.05). The mean content of noradrenaline and adrenaline was consistently higher in RV than LV tissue. Within the LV, however, neither preconditioning nor prolonged ischaemia had any significant effect upon tissue catecholamine content at any time in the experimental protocol.
Depletion of myocardial catecholamines is not involved in the mechanism of anti-arrhythmic protection by ischaemic preconditioning in isolated rat hearts.
本研究探讨缺血预处理的抗心律失常保护机制是否涉及心肌儿茶酚胺的耗竭。
在一系列随机研究中，用全血灌注的离体大鼠心脏，通过环绕左冠状动脉的圈套器诱导局部缺血和再灌注发作。对照心脏（第1组，n = 12）进行40分钟有氧灌注、30分钟缺血和10分钟再灌注。预处理心脏（第2组，n = 12）进行10分钟有氧灌注、三个缺血和再灌注周期（各5分钟）、30分钟缺血和10分钟再灌注。在缺血和再灌注的最后阶段连续记录心律并对心律失常进行量化。实验结束时，分离并冷冻右心室（RV；非缺血）和左心室（LV；缺血区域）组织样本。在另外5组（每组n = 6）中，在10分钟有氧灌注后、10分钟有氧灌注后接着进行1、2或3个预处理周期后以及40分钟有氧灌注后采集组织样本。分析所有组织样本中的儿茶酚胺含量。
预处理使缺血诱导的室颤发生率从第1组的67%降至第2组的8%，缺血诱导的室性心动过速发生率从100%降至17%，缺血诱导的室性早搏数量从246±25降至59±19（各P < 0.05）。右心室组织中去甲肾上腺素和肾上腺素的平均含量始终高于左心室组织。然而，在左心室内，预处理和长时间缺血在实验方案的任何时间对组织儿茶酚胺含量均无显著影响。
在离体大鼠心脏中，心肌儿茶酚胺的耗竭不参与缺血预处理的抗心律失常保护机制。
