Crozatier B, Franklin D, Theroux P, Tomoike H, Sasayama S, Ross J
Am J Physiol. 1977 Sep;233(3):H392-48. doi: 10.1152/ajpheart.1977.233.3.H392.
Postextrasystolic potentiation following coronary artery occlusion was studied serially using pairs of ultrasonic crystals to measure regional myocardial function in control, marginally ischemic, and ischemic segments of the left ventricle in dogs. Prior to coronary occlusion (CO), percent shortening in control (normal) segments increased by an average of 51.4 +/- 4.6% in the beat after a premature ventricular contraction (post-PVC beat), and this response changed little after coronary occlusion. During the 1st min after CO, in ischemic segments, systolic expansion developed but was replaced by active shortening in post-PVC beats; however, after 3 min of CO (average) and thereafter, there was no net positive shortening in post-PVC beats. In marginally ischemic segments early after CO, hypokinesia developed, but there was marked augmentation of percent shortening (208.6 +/- 32.6%) which persisted in post-PVC beats even after 2 h. It is concluded that loss of postextrasystolic potentiation occurs rapidly in ischemic regions after CO and is not indicative of irreversible damage; partially ischemic regions retain this mechanism for prolonged periods.
利用成对的超声晶体连续研究冠状动脉闭塞后的心搏后增强作用,以测量犬左心室对照、轻度缺血和缺血节段的局部心肌功能。在冠状动脉闭塞(CO)之前,对照(正常)节段的缩短百分比在室性早搏后的搏动(PVC后搏动)中平均增加51.4±4.6%,冠状动脉闭塞后这种反应变化不大。在CO后的第1分钟内,在缺血节段,收缩期扩张出现,但在PVC后搏动中被主动缩短所取代;然而,在CO(平均)3分钟及之后,PVC后搏动中没有净正性缩短。在CO后早期的轻度缺血节段,运动减弱出现,但缩短百分比显著增加(208.6±32.6%),即使在2小时后仍持续存在于PVC后搏动中。得出的结论是,CO后缺血区域的心搏后增强作用迅速丧失,并不表明存在不可逆损伤;部分缺血区域长时间保留这种机制。