Improved cardiac cell excitation with symmetrical biphasic defibrillator waveforms.

According to the most commonly accepted hypothesis, ventricular defibrillation is produced by exciting cells in a critical mass of the ventricle. For monophasic defibrillator waveforms, this hypothesis correctly predicts a direct correlation between defibrillation threshold in the transthoracic calf model and excitation threshold for extracellular field stimulation in the cultured cell model. To further test the hypothesis, we determined whether symmetrical biphasic waveforms, which reduce defibrillation threshold in the calf to approximately 65% of that of the corresponding monophasic waveform (14), decrease excitation threshold in the cultured cell model. Experiments were performed on 100- to 250-microns aggregates from 10- to 12-day-old chick embryos. Excitation threshold strength-duration curves obtained at extracellular potassium (Ko) = 6.5 mM and pacing interval of 1,000 ms showed a significant reduction for symmetrical biphasic rectangular waveforms, when compared with the corresponding monophasic waveforms for durations greater than 3 ms. At the rheobase, the threshold ratio between the biphasic and monophasic waveforms was 0.63 (SE = 0.02). Transmembrane potentials during stimulation showed that excitation takes place during the second portion of the biphasic waveform for intensities that are subthreshold for the monophasic waveform. The relative effectiveness of the biphasic waveform (5-ms duration) increases under "fibrillation conditions" of short pacing interval (300 ms) and high extracellular potassium (10.5 mM). These results show that symmetrical biphasic waveforms decrease excitation threshold in the cultured cell model and that the degree of threshold reduction is dependent on Ko and beat rate.

Mechanism of microwave sterilization in the dry state.

With an automated computerized temperature control and a specialized temperature measurement system, dry spores of Bacillus subtilis subsp. niger were treated with heat simultaneously in a convection dry-heat oven and a microwave oven. The temperature of the microwave oven was monitored such that the temperature profiles of the spore samples in both heat sources were nearly identical. Under these experimental conditions, we unequivocally demonstrated that the mechanism of sporicidal action of the microwaves was caused solely by thermal effects. Nonthermal effects were not significant in a dry microwave sterilization process. Both heating systems showed that a dwelling time of more than 45 min was required to sterilize 10(5) inoculated spores in dry glass vials at 137 degrees C. The D values of both heating systems were 88, 14, and 7 min at 117, 130, and 137 degrees C, respectively. The Z value was estimated to be 18 degrees C.

Microlesion formation in myocardial cells by high-intensity electric field stimulation.

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.