Delhaas T, Arts T, Prinzen F W, Reneman R S
Department of Physiology, University of Maastricht, The Netherlands.
Am J Physiol. 1996 Dec;271(6 Pt 2):H2411-20. doi: 10.1152/ajpheart.1996.271.6.H2411.
During normoxia, asynchronous electrical activation of the left ventricle significantly affects regional mechanical performance. Regional fiber strain and external work during the ejection phase are found to be lower in early-activated than in late-activated regions. Because electrical activation is known to be delayed during ischemia, the present study was designed to investigate the influence of this electrical asynchrony on regional fiber strain, if any, during moderate and severe myocardial ischemia. Regional electrical activation time (t(ea)) and fiber strain during the ejection phase (ef,e) were measured in the epicardial layers of the left ventricular anterior wall during normoxia and after 15 min of total occlusion (n = 5) or 30, 60, 120, and 180 min of partial occlusion of the left anterior interventricular coronary artery (LAICA; n = 11). Myocardial blood flow (MBF) was assessed with radioactive microspheres. Blood gases, pH, and lactate and Pi contents were determined in arterial, local venous, and coronary sinus blood. During normoxia, t(ea) and ef,e were similar in various epicardial regions of the left ventricular anterior wall. During total LAICA occlusion, in the ischemic area, subepicardial MBF decreased from 0.86 +/- 0.36 (SD) to 0.18 +/- 0.09 ml.g-1.min-1 and subepicardial ef,e decreased from -0.11 +/- 0.02 to -0.01 +/- 0.01, whereas the delay in t(ea) between the normoxic basal-lateral and ischemic apical-medial areas increased slightly but significantly from 1.9 +/- 8.0 to 7.5 +/- 8.0 ms. After a 180-min partial occlusion of the LAICA, in the ischemic area, subepicardial MBF decreased from 0.62 +/- 0.17 to 0.49 +/- 0.18 ml.g-1.min-1 and ef,e decreased from -0.08 +/- 0.01 to -0.03 +/- 0.01. No significant change in the difference in t(ea) between the normoxic and ischemic areas could be detected (5.1 +/- 4.8 and 5.2 +/- 5.8 ms in the control situation and after 180-min partial occlusion, respectively). These findings indicate that in the ischemic epicardium 1) mechanical function is more affected than electrical impulse conduction and 2) delayed activation, if any, is accompanied by decreased instead of increased fiber strain, as found in the normoxic left ventricle.
在正常氧合状态下,左心室的异步电激活显著影响局部机械性能。研究发现,在射血期,早期激活区域的局部纤维应变和外部做功低于晚期激活区域。由于已知缺血时电激活会延迟,因此本研究旨在探讨这种电不同步在中度和重度心肌缺血期间对局部纤维应变的影响(如有)。在正常氧合状态下以及左前降支冠状动脉(LAICA)完全闭塞15分钟后(n = 5)或部分闭塞30、60、120和180分钟后(n = 11),测量左心室前壁心外膜层的局部电激活时间(t(ea))和射血期纤维应变(ef,e)。用放射性微球评估心肌血流量(MBF)。测定动脉血、局部静脉血和冠状窦血中的血气、pH值、乳酸和无机磷含量。在正常氧合状态下,左心室前壁不同心外膜区域的t(ea)和ef,e相似。在LAICA完全闭塞期间,在缺血区域,心外膜下MBF从0.86±0.36(标准差)降至0.18±0.09 ml·g-1·min-1,心外膜下ef,e从-0.11±0.02降至-0.01±0.01,而正常氧合状态下基底部外侧和缺血区域心尖部内侧之间的t(ea)延迟从1.9±8.0略微但显著增加至7.5±8.0毫秒。在LAICA部分闭塞180分钟后,在缺血区域,心外膜下MBF从0.62±0.17降至0.49±0.18 ml·g-1·min-1,ef,e从-0.08±0.01降至-0.03±0.01。在正常氧合和缺血区域之间未检测到t(ea)差异有显著变化(对照情况和180分钟部分闭塞后分别为5.1±4.8和5.2±5.8毫秒)。这些发现表明,在缺血的心外膜中,1)机械功能比电冲动传导受影响更大;2)如果存在激活延迟,伴随的是纤维应变降低而非增加,这与正常氧合的左心室情况不同。