Martin G B
Ann Emerg Med. 1984 Sep;13(9 Pt 2):846-8. doi: 10.1016/s0196-0644(84)80457-6.
Calcium antagonists have been shown to protect the myocardium against the deleterious effects of ischemia and reperfusion in both focal and global models. The mechanism of this protection is probably related to their ability to decrease the rapid and massive cytosolic and mitochondrial calcium overloading that occurs with reperfusion of severely ischemic myocardium. This calcium overloading uncouples oxidative phosphorylation, preventing repletion of ischemia-depleted ATP stores. The mode of action of calcium antagonists in protecting heart muscle is complex, and may ultimately depend on their ability to preserve sufficient energy to maintain intracellular ionic homeostasis. The cellular events that occur with prolonged cardiac ischemia have been well documented in animal studies, and are reflected in the clinical picture of electromechanical dissociation (EMD). ATP production is decreased during ischemia and quickly results in depleted energy stores. The electrical and mechanical activities of the heart are energy-consuming processes that gradually come to a halt in the presence of prolonged ischemia. In excised totally ischemic hearts, electrical activity persists for a time after contractions have ceased, resulting in the clinical picture of EMD. Eventually electrical activity stops as well, causing asystole. Calcium antagonists administered during resuscitation from EMD, as well as other terminal arrhythmias, may protect the myocardium from reperfusion injury and preserve the ATP stores necessary for normal cardiac function.
在局灶性和整体性模型中，钙拮抗剂已被证明可保护心肌免受缺血和再灌注的有害影响。这种保护机制可能与其降低严重缺血心肌再灌注时发生的快速且大量的胞质和线粒体钙超载的能力有关。这种钙超载会使氧化磷酸化解偶联，阻止缺血耗尽的ATP储备的补充。钙拮抗剂保护心肌的作用方式很复杂，最终可能取决于它们维持足够能量以维持细胞内离子稳态的能力。长时间心脏缺血时发生的细胞事件在动物研究中已有充分记录，并反映在电机械分离（EMD）的临床症状中。缺血期间ATP生成减少，并迅速导致能量储备耗尽。心脏的电活动和机械活动是耗能过程，在长时间缺血的情况下会逐渐停止。在离体完全缺血的心脏中，收缩停止后电活动仍会持续一段时间，从而导致EMD的临床症状。最终电活动也会停止，导致心脏停搏。在从EMD以及其他终末期心律失常复苏期间给予钙拮抗剂，可能会保护心肌免受再灌注损伤，并保留正常心脏功能所需的ATP储备。
