Lew W Y, Ban-Hayashi E
Circulation. 1985 Nov;72(5):1125-34. doi: 10.1161/01.cir.72.5.1125.
We examined the influence of left ventricular end-diastolic pressure (LVEDP) on the mechanical interaction between ischemic and nonischemic areas during acute myocardial ischemia. Circumferentially oriented ultrasonic segment gauges were implanted in the midwall of the anterior apex and posterior apex of the left ventricle in seven anesthetized dogs. Stroke volume was measured with a flow probe around the ascending aorta in five of these animals. We varied LVEDP with vena caval occlusion and dextran infusions to three matched levels (7, 12, and 19 mm Hg) before and 30 min after complete occlusion of the mid left anterior descending coronary artery. With acute ischemia, the anterior apex or ischemic zone demonstrated marked segmental lengthening during isovolumetric systole (end-diastole to aortic valve opening) and akinesis during the ejection phase (aortic valve opening to closure). In the posterior apex or nonischemic area, isovolumetric shortening increased and ejection phase shortening decreased during acute ischemia when compared with those under control conditions at the same LVEDP. Thus, a portion of the shortening generated by the nonischemic area was expended in stretching the ischemic zone during isovolumetric systole, thereby reducing the amount of ejection phase shortening. As LVEDP was increased, there was a parallel decrease in both the amount of isovolumetric lengthening in the ischemic zone and the isovolumetric shortening in the nonischemic area. As a result, acute ischemia produced less of a reduction in ejection phase shortening in the nonischemic area and in stroke volume at high as compared with low LVEDP. We conclude that the ischemic zone imposes a mechanical disadvantage on the nonischemic area, the magnitude of which is directly proportional to the amount of isovolumetric lengthening or bulge in the ischemic zone. An increase in LVEDP during acute ischemia improves regional and global ventricular function by both the Frank-Starling mechanism in the nonischemic (but not the ischemic) area and by reducing the mechanical disadvantage that the ischemic zone imposes on the nonischemic area.
我们研究了急性心肌缺血期间左心室舒张末期压力（LVEDP）对缺血区和非缺血区之间机械相互作用的影响。在七只麻醉犬的左心室前尖和后尖的中层壁植入周向取向的超声节段测量仪。其中五只动物通过围绕升主动脉的流量探头测量每搏输出量。在完全闭塞左前降支冠状动脉之前和之后30分钟，我们通过腔静脉闭塞和右旋糖酐输注将LVEDP改变为三个匹配水平（7、12和19 mmHg）。急性缺血时，前尖或缺血区在等容收缩期（舒张末期至主动脉瓣开放）表现出明显的节段性延长，在射血期（主动脉瓣开放至关闭）表现为运动不能。与相同LVEDP下的对照条件相比，急性缺血时后尖或非缺血区的等容缩短增加，射血期缩短减少。因此，非缺血区产生的一部分缩短在等容收缩期用于拉伸缺血区，从而减少射血期缩短的量。随着LVEDP升高，缺血区等容延长的量和非缺血区等容缩短的量均平行下降。结果，与低LVEDP相比，急性缺血在高LVEDP时对非缺血区射血期缩短和每搏输出量的降低作用较小。我们得出结论，缺血区给非缺血区带来机械劣势，其程度与缺血区等容延长或膨出的量成正比。急性缺血期间LVEDP的增加通过非缺血区（而非缺血区）的Frank-Starling机制以及减少缺血区对非缺血区施加的机械劣势来改善局部和整体心室功能。
