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Electrical stimulation with Pt electrodes. VII. Dissolution of Pt electrodes during electrical stimulation of the cat cerebral cortex.

Procedures are described for determining trace quantities of Pt released into brain tissue directly beneath cortical surface stimulation electrodes. Implanted electrodes (1.1 mm Pt discs) were stimulated for 4.5 h, 9 h and 36 h (4 X 9 h/day) with balanced biphasic pulses (20 micro C/cm2 or 100 micro C/cm2 per phase, 50 Hz), following which tissue 0-2 mm beneath stimulation electrodes and the encapsulating tissue adherent to electrodes was excised and analyzed for Pt. A time-dependent increase in Pt concentration was observed between 4.5 h (4-20 ng Pt/stimulation site) and 9 h (50-339 ng Pt/site) of stimulation at 100 micro C/cm2 with nearly all of the Pt located in the encapsulating tissue associated with the electrodes. Somewhat less Pt was observed in the 36 h samples, and it was almost equally distributed between the encapsulating tissue of the electrodes and the first millimeter depth of underlying brain tissue. Little or no Pt was found at electrode sites receiving 20 micro C/cm2 pulses. Control brain tissue samples as well as samples of blood, CSF and kidney were negative for Pt. The findings indicate that the rate of Pt dissolution gradually decreases during in vivo stimulation, and that dissolved Pt may slowly move away from stimulation sites, possibly by diffusion or fluid exchange.

Animals↗

Electrical activity generated in subicular and entorhinal cortices after electrical stimulation of the lateral and basolateral amygdala of the rat.

Evoked field potentials and extracellular unitary activity were recorded from entorhinal lateral and subicular ventral cortices under conditions of amygdala stimulation in equithesin-anesthetized rats. The stimulation of the lateral and basolateral nuclei of the amygdaloid complex evoked field potentials consisting of negative-positive waves in layers III-VI and positive-negative deflections in the superficial layers of the ventral subdivision of the entorhinal cortex. The stimulation of the lateral nucleus evoked similar potentials in the dorsal subdivision of this cortex. And the stimulation of the lateral and basolateral nuclei of the amygdala evoked negative-positive field potentials in layer III of the subicular cortex. Cellular activity of the entorhinal and subicular cells evoked by stimulation of the lateral and basolateral nuclei consisted of an excitatory response followed by a prolonged suppression period. This activation coincided with the negative potential recorded in the deeper layers of these cortices. Such observations provide support for amygdaloid projection to the entorhinal and subicular cortices as recent anatomical findings suggested. The functional significance of these observations indicate an amygdaloid influence on entorhinal-hippocampal neurotransmission as well as on the ventral subiculum which provides the major output from the hippocampus.

Amygdala↗

Monte Carlo simulation of the electrical differential capacitance of a double electrical layer formed at the heterogeneous metal oxide/electrolyte interface.

A semiempirical simulation study of differential capacitance c(d) is presented for the case in which the formula for the macroscopic surface potential is known. Both the differential capacity and the surface potential are treated as unique functions of the potential determining ions (H+ ions). The effects of surface heterogeneity on the surface charge density curves sigma0 = f(pH), and capacity curves c(d) = f(pH), as well as on the position of maximum capacitance are discussed. The "model" effects (influence of the model parameter on the results) are presented.

Journal Article↗

Extrasystolic beats affect transmural electrical dispersion during programmed electrical stimulation.

BACKGROUND: Experimental studies suggest that the electrocardiographic Tpeak-Tend (TpTe) interval reflects transmural dispersion of repolarization (TDR). The genesis and role of the TpTe interval in a clinical setting have not been established. This study aimed to assess the clinical usefulness of the TpTe interval as an index of TDR and a pro-arrhythmic marker. MATERIALS AND METHODS: Endocardial monophasic action potential (MAP) duration and electrocardiographic QTp, QTe and TpTe intervals were assessed in 13 patients undergoing an electrophysiological study. Surface electrocardiograms were recorded during right ventricular pacing (Basic Cycle Length = 600 ms) before and after single extrastimuli. RESULTS: Ventricular arrhythmia was induced in six patients. During ventricular pacing, MAP duration and QTp intervals shortened in response to extrastimuli applied at progressively shorter coupling intervals. In contrast, QTe intervals increased in response to premature stimulation and QTe dispersion increased at short coupling intervals. During sinus rhythm, the TpTe interval was greater in the inducible group in leads V3-V4. Premature stimulation increased the duration of TpTe intervals, suggesting an increase in TDR. The maximum TpTe interval was greater in the inducible than in the noninducible group, both during baseline ventricular drive pacing (163 +/- 22 vs. 130 +/- 27 ms, respectively, P < 0.03) and after application of shortly coupled extrastimuli (263 +/- 66 vs. 200 +/- 47 ms, respectively, P < 0.05). CONCLUSIONS: The TpTe interval of surface ECG is likely to represent TDR. TDR is increased by premature ventricular stimulation and the magnitude of the maximum TpTe interval (i.e. maximum TDR) during ventricular pacing is greater in patients with inducible arrhythmias.

Action Potentials↗