Postresuscitation stunning: postfibrillatory myocardial dysfunction caused by reduced myofilament Ca2+ responsiveness after ventricular fibrillation-induced myocyte Ca2+ overload.

作者: CHRISTIAN E. ZAUGG , ANDRE ZIEGLER , RANDALL J. LEE , VANIA BARBOSA , PETER T. BUSER

DOI: 10.1046/J.1540-8167.2002.01017.X

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摘要: Postresuscitation Myocardial Stunning.Introduction: Resuscitation from ventricular fibrillation (VF), particularly prolonged VF, frequently is complicated by postfibrillatory myocardial dysfunction (postresuscitation stunning). We tested whether this can be caused reduced myofilament Ca2+ responsiveness after VF-induced myocyte overload. also electrical defibrillation shocks contribute to dysfunction. Methods and Results: Myofilament was estimated as ratio of left developed pressure over transient amplitudes (assessed indo-1 fluorescence) in isolated perfused rat hearts before, during, VF (1.5 or 10 min) comparing three modes (biphasic shocks, lidocaine, spontaneous). found that, independent these modes, significantly reduced, although were not ischemic acidotic during (unchanged coronary flow, oxygen consumption, pH the effluent). This reduction associated with overload increasing decreasing (using 1 μM diltiazem 6 mM extracellular calcium) led parallel changes responsiveness. However, shock energy (range 0.1–15.0 J/g wet heart weight). Conclusion: Postfibrillatory Electrical (up 15 weight), however, do dysfunction. Our findings suggest that early additional therapy targeting intracellular may normalize partially prevent postresuscitation stunning.

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