Guyton R A, McClenathan J H, Michaelis L L
Am J Cardiol. 1977 Sep;40(3):381-92. doi: 10.1016/0002-9149(77)90160-6.
The temporal evolution of myocardial ischemia was studied in open chest dogs at constant preload, afterload and heart rate. In one group of animals, a variable circumflex arterial stenosis was used to maintain constant distal circumflex arterial hypotension (40 to 50 mm Hg). During a 3 hour period of stenosis, flow in the subendocardial fourth of the ischemic ventricular wall decreased from 0.22 to 0.09 ml/g per min (P less than 0.02), whereas subepicardial flow was not significantly changed. Local vascular resistance, therefore, doubled in the most ischemic area of myocardium. In a second group of animals in which proximal coronary stenosis was held constant and pressure varied, an ischemia-mediated increase in local vascular resistance was also demonstrated. In addition, a reciprocal relation was observed between changes in flow in the left anterior descending coronary region and changes in collateral flow to the region of the circumflex artery. A coronary steal mechanism and an ischemia-mediated resistance increase may be two means by which ischemia is self-propagating.
在开胸犬身上，在恒定的前负荷、后负荷和心率条件下研究了心肌缺血的时间演变。在一组动物中，使用可变的左旋支动脉狭窄来维持恒定的左旋支动脉远端低血压（40至50毫米汞柱）。在狭窄的3小时期间，缺血心室壁心内膜下四分之一处的血流从每分钟0.22毫升/克降至0.09毫升/克（P小于0.02），而心外膜血流没有显著变化。因此，心肌最缺血区域的局部血管阻力增加了一倍。在另一组近端冠状动脉狭窄保持恒定而压力变化的动物中，也证明了缺血介导的局部血管阻力增加。此外，观察到左前降支冠状动脉区域血流变化与左旋支动脉区域侧支血流变化之间存在相互关系。冠状动脉窃血机制和缺血介导的阻力增加可能是缺血自我传播的两种方式。
