Protection of the myocardium during myocardial infarction: pharmacologic protection during thrombolytic therapy.
Protection of the myocardium during myocardial infarction: pharmacologic protection during thrombolytic therapy.
复制标题
心肌梗死期间的心肌保护：溶栓治疗期间的药物保护。
DOI：
10.1016/0002-9149(90)90124-j
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发表时间：
1990
期刊：
影响因子：
--
通讯作者：
Buja,LM
中科院分区：
文献类型：
--
作者：
Willerson,JT;Buja,LM
在进展性心肌梗死的早期阶段，最有效的保护受损心肌的方法是再灌注。然而，再灌流可能会导致进一步的心肌损伤。心肌耗氧量的主要决定因素的改变，包括心率、收缩状态和心肌壁张力的增加，也可能增加梗塞面积。了解心肌梗死时心肌损伤演变的基本机制对于开发保护策略具有重要意义，这些保护策略可以缩小心肌梗死面积或减轻再灌注所致的心肌损伤，或两者兼而有之。选择性钙拮抗剂、β阻滞剂和磷脂酶拮抗剂或抑制剂可减少早期再灌注相关的心肌梗死面积。自由基清除剂和钙拮抗剂可减轻再灌注损伤。在最初的事件后，再梗塞的频率最终可能会通过药物策略来减少，这些药物策略干扰了激活的血小板和白细胞的黏附、聚集和介质释放，从而促进了血小板的进一步聚集或诱导冠状动脉血管收缩。保护策略包括血栓素受体拮抗剂和合成抑制剂，5-羟色胺受体拮抗剂，可能是白三烯合成抑制剂或受体拮抗剂，以及阿司匹林。未来的临床试验应该检验再灌注和选定的药物策略的联合疗效，这些药物策略在受损心肌中钙蓄积后，减轻β和α肾上腺素能机制以及氧自由基对受损心肌细胞的损伤作用，防止由血小板和血小板介质介导的再闭塞。
The most effective way to protect injured myocardium during the early phases of evolving myocardial infarction is with reperfusion. However, reperfusion may induce further myocardial injury. Alterations in the major determinants of myocardial oxygen demand, including increases in heart rate, contractile state and myocardial wall tension may also increase infarct size. An understanding of the basic mechanisms involved in the evolution of myocardial injury during myocardial infarction is important to the development of protective strategies that may reduce infarct size or attenuate reperfusion-induced myocardial injury, or both. Selective calcium antagonists, β blockers, and phospholipase antagonists or inhibitors may reduce infarct size in association with early reperfusion. Reperfusion injury may be attenuated by free radical scavengers and calcium antagonists. Reinfarction, after the initial event, may ultimately be reduced in frequency by pharmacologic strategies that interfere with platelet adhesion, aggregation, and mediator release from activated platelets and white cells that promote further platelet aggregation or induce coronary artery vasoconstriction. Included among protective strategies are thromboxane receptor antagonists and synthesis inhibitors, serotonin receptor antagonists, possibly leukotriene synthesis inhibitors or receptor antagonists, and aspirin. Future clinical trials should test the combined efficacy of reperfusion and selected pharmacologic strategies that after calcium accumulation in the injured myocardium, diminish the injurious effects of β- and α-adrenergic mechanisms and oxygen-derived free radicals on injured myocytes, and prevent reocclusion mediated by platelets and platelet mediators.