Microlesion formation in myocardial cells by high-intensity electric field stimulation.
Microlesion formation in myocardial cells by high-intensity electric field stimulation.
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高强度电场刺激心肌细胞形成微损伤。
DOI:
10.1152/ajpheart.1987.253.2.h480
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发表时间:
1987
期刊:
影响因子:
--
通讯作者:
Balasky,G
中科院分区:
文献类型:
--
作者:
Jones,JL;Jones,RE;Balasky,G
Arrhythmias, S-T segment changes, immediate refibrillation, and other signs of dysfunction are often observed after clinical and experimental transthoracic defibrillation. In vitro studies suggested that shock-induced dysfunction is induced by sarcolemmal dielectric breakdown accompanied by ionic exchanges through transient, shock-induced microlesions in the sarcolemma. To test this hypothesis, cultured chick embryo myocardial cells were shocked in media containing fluorescein isothiocyanate-labeled dextrans (FITC-dextrans) ranging in molecular mass from 4 to 70 kDa, using electric field stimulation 5 ms in duration and ranging in intensity from 0 to 200 V/cm. Results showed that the percentage of cells incorporating 4- to 20-kDa dextrans increased in a dose-dependent manner. The 4- and 10-kDa dextrans were incorporated beginning at intensities of 50–100 V/cm. Dextran incorporation corresponded with shock intensities which produced a shock-induced arrest of spontaneous contraction lasting 1 min. The 20-kDa dextrans were incorporated following 150- and 200-V/cm shocks. Shocks of these intensities also produced a transient postshock contracture. Larger dextrans (40 and 70 kDa) were not incorporated. These results suggest the formation of transient sarcolemmal microlesions having a diameter of 45-60 A during high-intensity electric field stimulation.