Buda A J, Zotz R J, Gallagher K P
Circulation. 1987 Jul;76(1):163-72. doi: 10.1161/01.cir.76.1.163.
During acute myocardial ischemia, there exists a zone of myocardial dysfunction that surrounds the central ischemic area that has been termed the functional border zone. We hypothesized that this nonischemic but dysfunctional myocardium may respond to an inotropic challenge. To address this issue, we studied 11 open-chest dogs during acute left circumflex (LCx) occlusion. Simultaneous two-dimensional echocardiograms and radioactive microsphere injections were used to create circumferential left ventricular flow-function maps at the papillary muscle level. Serial studies were performed at baseline, 15 min after LCx occlusion, and after the infusion of dobutamine during LCx occlusion. After occlusion, wall thickening decreased from 52 +/- 8% (mean +/- SEM) to -5 +/- 5% (p less than .01) in the central ischemic zone. The extent of left ventricular dysfunction measured 170 +/- 11 degrees while the subendocardial hypoperfusion zone was 130 +/- 9 degrees (p less than .05), resulting in a functional border zone of 40 +/- 11 degrees. During the infusion of dobutamine, wall thickening did not change in the central ischemic zone but increased adjacent to the functional border zone (p less than .01) and in the normal zone (p less than .05), reducing the extent of the functional border zone to 19 +/- 16 degrees (p less than .05). After dobutamine, the slope of transition of wall thickening from nonischemic to ischemic zones, measured directly from the left ventricular function map, increased on the free wall border (0.71 +/- 0.11 to 0.95 +/- 0.10, p less than .02) to a greater extent than on the septal border (0.60 +/- 0.08 to 0.73 +/- 0.06, p = .07). We conclude that nonischemic myocardium adjacent to ischemic tissue responds to inotropic challenge, dobutamine produces a significant decrease in the size of the functional border zone, and dynamic changes in wall thickening after inotropic intervention are greater in the functional border zone of the lateral free wall than at the septal border of the ischemic area.
在急性心肌缺血期间,存在一个心肌功能障碍区域,它围绕着中央缺血区,这个区域被称为功能边界区。我们假设这个非缺血但功能失调的心肌可能对正性肌力刺激有反应。为了解决这个问题,我们在11只开胸犬急性左旋支(LCx)闭塞期间进行了研究。同时使用二维超声心动图和放射性微球注射来创建乳头肌水平的圆周左心室血流-功能图。在基线、LCx闭塞后15分钟以及LCx闭塞期间输注多巴酚丁胺后进行系列研究。闭塞后,中央缺血区的室壁增厚从52±8%(平均值±标准误)降至-5±5%(p<0.01)。左心室功能障碍的范围为170±11度,而心内膜下灌注不足区为130±9度(p<0.05),导致功能边界区为40±11度。在输注多巴酚丁胺期间,中央缺血区的室壁增厚没有变化,但在功能边界区附近(p<0.01)和正常区(p<0.05)增加,使功能边界区的范围缩小至19±16度(p<0.05)。给予多巴酚丁胺后,直接从左心室功能图测量的室壁增厚从非缺血区到缺血区的过渡斜率在游离壁边界处增加(0.71±0.11至0.95±0.10,p<0.02),程度大于在间隔边界处(0.60±0.08至0.73±0.06,p = 0.07)。我们得出结论,缺血组织附近的非缺血心肌对正性肌力刺激有反应,多巴酚丁胺可使功能边界区的大小显著减小,并且正性肌力干预后室壁增厚的动态变化在外侧游离壁的功能边界区比在缺血区的间隔边界处更大。