Stimulatory current at the edge of an inactive conductor in an electric field: role of nonlinear interfacial current-voltage relationship.

Cardiac electric field stimulation is critical for the mechanism of defibrillation. The presence of certain inactive epicardial conductors in the field during defibrillation can decrease the defibrillation threshold. We hypothesized this decrease is due to stimulatory effects of current across the interface between the inactive conductor and the heart during field stimulation. To examine this current and its possible stimulatory effects, we imaged transmittance of indium-tin-oxide (ITO) conductors, tested for indium with X-ray diffraction, created a computer model containing realistic ITO interfacial properties, and optically mapped excitation of rabbit heart during electric field stimulation in the presence of an ITO conductor. Reduction of indium decreased transmittance at the edge facing the anodal shock electrode when trans-interfacial voltage exceeded standard reduction potential. The interfacial current-voltage relationship was nonlinear, producing larger conductances at higher currents. This nonlinearity concentrated the interfacial current near edges in images and in a computer model. The edge current was stimulatory, producing early postshock excitation of rabbit ventricles. Thus, darkening of ITO indicates interfacial current by indium reduction. Interfacial nonlinearity concentrates current near the edge where it can excite the heart. Stimulatory current at edges may account for the reported decrease in defibrillation threshold by inactive conductors.

Epicardial conductors can lower the defibrillation threshold in rabbit hearts.

During a defibrillation shock, epicardial conductors can introduce antistimulatory effects due to lowering of the voltage gradient in myocardial tissue under the conductor and stimulatory effects due to membrane polarization near edges. We hypothesized that increasing the area of conductors increases the defibrillation threshold (DFT), while increasing the amount of stimulatory edge of conductors decreases the DFT. To test this, we measured the DFT in excised rabbit hearts with and without sets of rectangular conductors having 250 or 500 mm(2) area and 100, 200, or 400 mm length of edges perpendicular to the line intersecting the shock electrodes. Unlike previous reports in which conductors increased or did not change DFT, present results indicate a conductor geometry having area of 250 mm (2) and edge of 200 mm decreases the DFT. This result is consistent with the hypothesis that stimulatory effects of the edge of a conductor can enhance defibrillation shock efficacy.

Noninvasive assessment of the effects of glucagon on the gastric slow wave.

Hyperglycemic effects on the gastric slow wave are not well understood, and no studies have examined the effects that hyperglycemia has on gastric slow wave magnetic fields. We recorded multichannel magnetogastrograms (MGGs) before and after intravenous administration of glucagon and subsequent modest hyperglycemia in 20 normal volunteers. Normal slow waves were evident in baseline MGG recordings from all 20 subjects, but within 15 min after glucagon had been given, we noted significant effects on MGG signals. In addition to an overall decrease in the slow wave frequency from 2.9 +/- 0.5 cycles per min (cpm) to 2.2 +/- 0.1 cpm (P < 0.05), we observed significant changes in the number and range of spectral peaks recorded. Furthermore, the propagation velocity determined from surface current density maps computed from the multichannel MGG decreased significantly (7.1 +/- 0.8 mm/s to 5.0 +/- 0.3 mm/s, P < 0.05). This is the first study of biomagnetic effects of hyperglycemia in normal subjects. Our results suggest that the analysis of the MGG provides parameter quantification for gastric electrical activity specific to and characteristic of slow wave abnormalities associated with increased serum glucose by injection of glucagon.