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尽管存在持续性收缩功能障碍,但缺血后顿抑心肌的电生理恢复。

Electrophysiologic recovery in postischemic, stunned myocardium despite persistent systolic dysfunction.

作者信息

Hanich R F, Levine J H, Prood C, Weiss J L, Callans D J, Spear J F, Moore E N

机构信息

Department of Animal Biology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia 19104.

出版信息

Am Heart J. 1993 Jan;125(1):23-32. doi: 10.1016/0002-8703(93)90052-b.

Abstract

Previous investigators have hypothesized that myocardial "stunning" may result either from a primary impairment in excitation or from electromechanical dissociation. Thrombolytic therapy and angioplasty have increased the importance of understanding the electrophysiologic effects of brief ischemia followed by reperfusion. We investigated the electrophysiologic properties of mechanically dysfunctional stunned myocardium in 18 dogs anesthetized with pentobarbital (30 mg/kg, intravenously administered). After thoracotomy, the proximal anterior descending coronary artery was occluded for 15 minutes, which was followed by 20 minutes of reperfusion. At baseline, peak ischemia, and 20 minutes of reperfusion, local electrogram durations, activation times, and refractory periods were measured from 12 standardized sites within the ischemic and border zones. Echocardiographic percentage of systolic wall thickening confirmed normal preischemic and markedly reduced postischemic function in the investigated region. Despite the marked electrophysiologic abnormalities observed in the ischemic zone during ischemia, mean electrogram duration, calculated conduction velocity, and mean effective refractory period after 20 minutes of reperfusion had returned almost to baseline values 39.2 +/- 11.5 msec versus 37.2 +/- 12.1 msec, 0.65 +/- 0.15 m/sec versus 0.68 +/- 0.15 m/sec, and 134 +/- 14 msec versus 131 +/- 8 msec, respectively. Corresponding mean values within the ischemic border zone were similarly close to baseline values after reperfusion. There was no significant difference in local heterogeneity (coefficient of variation) within the ischemic or border zone after reperfusion versus baseline values. Although the postischemic electrophysiologic status returned to normal, systolic thinning and dyskinesis persisted in the region of measurement. The contractile dysfunction that results from reperfusion-induced injury can thus occur in the setting of apparent excitation-contraction uncoupling.

摘要

先前的研究人员推测,心肌“顿抑”可能源于兴奋的原发性损害或电机械分离。溶栓治疗和血管成形术增加了理解短暂缺血后再灌注的电生理效应的重要性。我们研究了18只戊巴比妥(30mg/kg,静脉注射)麻醉的犬机械功能失调的顿抑心肌的电生理特性。开胸后,将冠状动脉前降支近端闭塞15分钟,随后再灌注20分钟。在基线、缺血高峰期和再灌注20分钟时,从缺血区和边缘区内12个标准化部位测量局部心电图持续时间、激活时间和不应期。超声心动图测量的收缩期室壁增厚百分比证实,研究区域缺血前功能正常,缺血后功能明显降低。尽管在缺血期间缺血区观察到明显的电生理异常,但再灌注20分钟后的平均心电图持续时间、计算的传导速度和平均有效不应期几乎恢复到基线值,分别为39.2±11.5毫秒对37.2±12.1毫秒、0.65±0.15米/秒对0.68±0.15米/秒、134±14毫秒对131±8毫秒。再灌注后缺血边缘区内的相应平均值同样接近基线值。再灌注后缺血区或边缘区内的局部异质性(变异系数)与基线值相比无显著差异。尽管缺血后的电生理状态恢复正常,但测量区域仍存在收缩期变薄和运动障碍。因此,再灌注诱导损伤导致的收缩功能障碍可在明显的兴奋-收缩解偶联情况下发生。

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