The Role of Beta-1 Receptors in the Response to Myocardial Ischemia

The Role of Beta-1 Receptors in the Response to Myocardial Ischemia

Acute myocardial ischemia is commonly diagnosed by ST-segment deviations. These deviations, however, can show a paradoxical recovery even in the face of ongoing ischemic stress. A possible mechanism for this response may be the cardio-protective effects of the autonomic nervous system (ANS) via beta-1 receptors. We assessed the role of norepinephrine (NE), a beta-1 agonist, and esmolol (ES), a beta-1 antagonist, in the recovery of ST-segment deviations during myocardial ischemia. We used an experimental model of controlled myocardial ischemia in which we simultaneously recorded electrograms intramurally and on the epicardial surface. We measured ischemia as deviations in the potentials measured at 40% of the ST-segment duration. During control intervention, 27% of epicardial electrodes showed no ischemic ST-segment deviations, whereas during the interventions with NE and ES, 100% of epicardial electrodes showed no ischemic ST-segment deviations. Intramural electrodes revealed a different behavior with 71% of electrodes showing no ischemic ST-segment deviations during control ischemia, increasing to 79% and 82% for NE infusion and ES infusion interventions, respectively. These preliminary results suggest that recovery of intramural regions of the heart is delayed by the presence of both beta-1 agonists and antagonists even as epicardial potentials show almost complete recovery.

急性心肌缺血通常通过ST段偏移来诊断。然而，即使在持续缺血应激的情况下，这些偏移也可能出现矛盾性恢复。这种反应的一个可能机制是自主神经系统（ANS）通过β -1受体产生的心脏保护作用。我们评估了去甲肾上腺素（NE，一种β -1激动剂）和艾司洛尔（ES，一种β -1拮抗剂）在心肌缺血期间ST段偏移恢复中的作用。我们使用了一种可控心肌缺血的实验模型，在该模型中我们同时记录心内膜下和心外膜表面的心电图。我们将缺血测量为在ST段持续时间的40%处测量的电位偏移。在对照干预期间，27%的心外膜电极未显示缺血性ST段偏移，而在使用NE和ES干预期间，100%的心外膜电极未显示缺血性ST段偏移。心内膜下电极表现出不同的行为，在对照缺血期间71%的电极未显示缺血性ST段偏移，在NE输注和ES输注干预时分别增加到79%和82%。这些初步结果表明，即使心外膜电位几乎完全恢复，β -1激动剂和拮抗剂的存在都会延迟心脏心内膜下区域的恢复。