Zaugg Christian E, Ziegler André, Lee Randall J, Barbosa Vânia, Buser Peter T
Department of Research, University Hospital Basel, Switzerland.
J Cardiovasc Electrophysiol. 2002 Oct;13(10):1017-24. doi: 10.1046/j.1540-8167.2002.01017.x.
Resuscitation from ventricular fibrillation (VF), particularly from prolonged VF, frequently is complicated by postfibrillatory myocardial dysfunction (postresuscitation stunning). We tested whether this dysfunction can be caused by reduced myofilament Ca2+ responsiveness after VF-induced myocyte Ca2+ overload. We also tested whether electrical defibrillation shocks contribute to this dysfunction.
Myofilament Ca2+ responsiveness was estimated as ratio of left ventricular developed pressure over myocyte Ca2+ transient amplitudes (assessed as indo-1 fluorescence) in isolated perfused rat hearts before, during, and after VF (1.5 or 10 min) comparing three modes of defibrillation (biphasic electrical shocks, lidocaine, or spontaneous). We found that, independent of these defibrillation modes, myofilament Ca2+ responsiveness was significantly reduced, particularly after prolonged VF, although hearts were not ischemic or acidotic during and after VF (unchanged coronary flow, myocardial oxygen consumption, and pH of the coronary effluent). This reduction was associated with VF-induced myocyte Ca2+ overload and increasing or decreasing Ca2+ overload during VF (using 1 microM diltiazem or 6 mM extracellular calcium) led to parallel changes of myofilament Ca2+ responsiveness. However, myofilament Ca2+ responsiveness was not associated with the defibrillation shock energy (range 0.1-15.0 J/g wet heart weight).
Postfibrillatory myocardial dysfunction can be caused by reduced myofilament Ca2+ responsiveness after VF-induced myocyte Ca2+ overload. Electrical defibrillation shocks (up to 15 J/g wet heart weight), however, do not significantly contribute to this dysfunction. Our findings suggest that early additional therapy targeting intracellular Ca2+ overload may normalize myocyte Ca2+ and partially prevent postresuscitation stunning.
室颤（VF）复苏，尤其是长时间室颤复苏，常并发纤颤后心肌功能障碍（复苏后心肌顿抑）。我们测试了这种功能障碍是否由室颤诱导的心肌细胞钙超载后肌丝钙反应性降低所致。我们还测试了电除颤电击是否导致这种功能障碍。
在离体灌注大鼠心脏室颤（1.5或10分钟）前、期间和之后，通过比较三种除颤模式（双相电击、利多卡因或自发恢复），将肌丝钙反应性估计为左心室发育压力与心肌细胞钙瞬变幅度（以indo-1荧光评估）之比。我们发现，无论这些除颤模式如何，肌丝钙反应性均显著降低，尤其是在长时间室颤后，尽管在室颤期间和之后心脏无缺血或酸中毒（冠状动脉血流、心肌氧消耗和冠状动脉流出液pH值无变化）。这种降低与室颤诱导的心肌细胞钙超载相关，并且在室颤期间增加或减少钙超载（使用1微摩尔地尔硫䓬或6毫摩尔细胞外钙）导致肌丝钙反应性平行变化。然而，肌丝钙反应性与除颤电击能量（范围为0.1 - 15.0焦耳/克湿心重）无关。
纤颤后心肌功能障碍可由室颤诱导的心肌细胞钙超载后肌丝钙反应性降低引起。然而，电除颤电击（高达15焦耳/克湿心重）对这种功能障碍无显著影响。我们的研究结果表明，早期针对细胞内钙超载的额外治疗可能使心肌细胞钙正常化，并部分预防复苏后心肌顿抑。
