Kirk E S, Sonnenblick E H
Am Heart J. 1982 Apr;103(4 Pt 2):756-67. doi: 10.1016/0002-8703(82)90483-5.
A model of myocardial ischemia based on the balance of oxygen demand and supply is presented. Ischemia is invariably the result of a limited coronary blood flow (supply), but increased oxygen consumption is often cited as a factor causing an imbalance of demand and supply. The role of contractility in ischemia, however, has been overemphasized, and inotropic agents such as glycosides and isoproterenol frequently have effects on supply that overshadow their effects on myocardial oxygen consumption. With deep ischemia leading to infarction, supply also tends to overshadow demand in determining the extent of transmural necrosis. Moreover, the anatomic pattern of supply precisely delineates both the region at risk following coronary occlusion and the ultimate extent of the infarction. These views are presented in anatomic models of myocardial ischemia and infarction.
提出了一种基于氧供需平衡的心肌缺血模型。缺血总是冠状动脉血流受限（供应不足）的结果，但氧消耗增加常被认为是导致供需失衡的一个因素。然而，收缩性在缺血中的作用被过度强调了，洋地黄苷和异丙肾上腺素等正性肌力药物对供应的影响往往掩盖了它们对心肌氧消耗的影响。随着深度缺血导致梗死，在决定透壁坏死范围时，供应也往往超过需求。此外，供应的解剖模式精确地描绘了冠状动脉闭塞后危险区域以及梗死的最终范围。这些观点在心肌缺血和梗死的解剖模型中得到了阐述。
