Academic literature on the topic 'Rate Of Rise Of Recovery Voltage (RRRV)'

In the study, an interrupting performance test on the 145 kV gas circuit breaker is performed according to three different gases: SF6, g3 (5% NovecTM4710 with 95% CO2), and CO2(70%)/O2(30%) gases. Thanks to research advancements, it is confirmed that CO2 and g3 (5% NovecTM 4710) gases, respectively, have 40% and 75% dielectric strength, compared to that of SF6 gas. The filling pressure and transient recovery voltage criteria of each gas were determined differently in order to compare the maximum interrupting performance of each gas. The pressure of SF6 gas was determined to be 5.5 bar, which is typically used in circuit breakers. The pressure of the other two gases was determined to be 8.0 bar (the maximum available pressure of the test circuit breaker) to find the maximum interrupting performance. Moreover, the rate-of-rise of transient recovery voltage of SF6 was determined as 10 kV/μs, which is the value at the state of maximum interrupting performance of the test circuit breaker with SF6. On the other hand, the rate-of-rise of transient recovery voltages of g3 (5% NovecTM4710 with 95% CO2) and CO2(70%)/O2(30%) gases were, respectively, determined as 4∼5 kV/μs to find the interruption available point. The characteristics of arc conductance, arc current, and arc voltage near the current zero, and post-arc current are analyzed to compare the interrupting performance, according to different arc-quenching gases. The arc current is measured using a current transformer (Rogowski coil), and a signal processing method of the arc current and arc voltage is introduced to increase the reliability of the interrupting performance results. As a result of the test, it is confirmed that the critical arc conductance for all test conditions converged within a certain range and the value is around 0.7 mS. In addition, the critical current slope just before the current zero-crossing during the interrupting process is shown to be 1.8 A/μs between interruption success and failure. Consequently, it is verified that the CO2(70%)/O2(30%) mixture and g3 (5% NovecTM4710 with 95% CO2) have a similar arc extinguishing performance and SF6 has a relatively higher extinguishing performance than that of CO2(70%)/O2(30%) mixture and g3 (5% NovecTM4710 with 95% CO2) under the aforementioned filling pressure and TRV conditions.

Exposure to CO2 acidifies the cytosol of mitochondria-rich cells in turtle bladder epithelium. The result of the decrease in pH in these, the acid-secreting cells of the epithelium, is a transient increase in cell calcium, which causes exocytosis of vesicles containing proton-translocating ATPase. Because mitochondria-rich cells have rapid luminal membrane turnover, we were able to identify single mitochondria-rich cells by their endocytosis of rhodamine-tagged albumin. Using fluorescence emission of 5,6-carboxyfluorescein at two excitation wavelengths, we measured cell pH in these identified mitochondria-rich cells and found that although the cell pH fell, it recovered within 5 min despite continuous exposure to CO2. This pH recovery also occurred at the same rate in Na+-free media. However, pH recovery did not occur when luminal pH was 5.5, a condition under which the H+-pump does not function, suggesting that recovery of cell pH is due to the luminally located H+ ATPase. Chelation of extracellular calcium by EGTA prevented the CO2-induced rise in cell calcium measured with the intracellular fluorescent dyes Quin 2 or Fura 2 and also prevented recovery of cell pH. When the change in cell calcium was buffered by loading the cells with high concentrations of Quin 2, the CO2-induced decrease in pH did not return back to basal levels. We had found previously that buffering intracellular calcium transients prevented CO2-stimulated exocytosis. Further, we show here that the increased H+ current in voltage-clamped turtle bladders, which is directly proportional to the number of H+-pump-containing vesicles that fuse with the luminal membrane, was significantly reduced in calcium-depleted bladders. These results suggest that pH regulation in these acid-secreting cells occurs by calcium-dependent exocytosis of vesicles containing proton pumps, whose subsequent turnover restores the cell pH to its initial levels.

To investigate the mechanisms by which low intracellular pH influences calcium signaling, I have injected HCl, and in some experiments CaCl2, into snail neurons while recording intracellular pH (pHi) and calcium concentration ([Ca2+]i) with ion-sensitive microelectrodes. Unlike fluorescent indicators, these do not increase buffering. Slow injections of HCl (changing pHi by 0.1–0.2 pH units min−1) first decreased [Ca2+]i while pHi was still close to normal, but then increased [Ca2+]i when pHi fell below 6.8–7. As pHi recovered after such an injection, [Ca2+]i started to fall but then increased transiently before returning to its preinjection level. Both the acid-induced decrease and the recovery-induced increase in [Ca2+]i were abolished by cyclopiazonic acid, which empties calcium stores. Caffeine with or without ryanodine lowered [Ca2+]i and converted the acid-induced fall in [Ca2+]i to an increase. Injection of ortho-vanadate increased steady-state [Ca2+]i and its response to acidification, which was again blocked by CPA. The normal initial response to 10 mM caffeine, a transient increase in [Ca2+]i, did not occur with pHi below 7.1. When HCl was injected during a series of short CaCl2 injections, the [Ca2+]i transients (recorded as changes in the potential (VCa) of the Ca2+-sensitive microelectrode), were reduced by only 20% for a 1 pH unit acidification, as was the rate of recovery after each injection. Calcium transients induced by brief depolarizations, however, were reduced by 60% by a similar acidification. These results suggest that low pHi has little effect on the plasma membrane calcium pump (PMCA) but important effects on the calcium stores, including blocking their response to caffeine. Acidosis inhibits spontaneous calcium release via the RYR, and leads to increased store content which is unloaded when pHi returns to normal. Spontaneous release is enhanced by the rise in [Ca2+]i caused by inhibiting the PMCA.

1. We characterized the kinetics of presynaptic Ca2+ ion concentration in optic nerve fibers and terminals of the optic tectum in Rana pipiens with the use of microfluorimetry. Isolated frog brains were incubated with the membrane-permeant tetraacetoxymethyl ester (AM) of the Ca2+ indicator fura-2. An optic nerve shock caused a transient decrease in the 380-nm excited fluorescence in the optic tectum with a rise time of <15 ms and a recovery to prestimulus levels on a time scale of seconds. 2. In normal saline, the amplitude of the fluorescence transients was dependent on stimulus intensity and at all levels it was directly correlated with the amplitude of postsynaptic field potentials produced by activation of unmyelinated optic nerve fibers. In the presence of the non-N-methyl-D-aspartate glutamate receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione, the amplitude and time course of fluorescence transients remained essentially unchanged while postsynaptic field potential amplitude was greatly reduced. Replacing extracellular Ca2+ with Ba2+ blocked unfacilitated postsynaptic field potentials while fluorescence transients remained significant. In reduced-Ca2+ salines (<1 mM), the amplitude of fluorescence transients increased approximately linearly with extracellular [Ca2+], whereas the amplitude the corresponding field potential was nonlinearly related to the fluorescent transient amplitude (approximately 2.5 power). In thin sections of labeled tecta, fluorescence labeling was localized to 1-micron puncta in the termination zone of optic nerve fibers in the superficial layers. Taken together, these results provide strong evidence that the fluorescence transients correspond to an increase in Ca2+ in presynaptic terminals of unmyelinated optic nerve fibers. 3. During trains of optic nerve stimulation, the amplitude of fluorescence transients to succeeding action potentials became smaller. The decrement of the amplitudes was not observed in mag-fura-5-labeled tecta, when the intracellular Ca2+ buffering capacity of fura-2-labeled terminals was increased by incubation with bis-(o-aminophenoxy)-N,N,N',N'-tetraacetic acid (BAPTA)-AM or ethylene glycol-bis (beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA)-AM, or in low-Ca2+ saline. We conclude that the Ca2+ influx per action potential is constant during the train and that the reduced response was produced by saturation of the fura-2. We provide a mathematical analysis of this saturation effect and use it to estimate the Ca2+ change per action potential. 4. Both BAPTA-AM and EGTA-AM reduced the overall amplitude of fura-2-measured Ca2+ transients and reduced the saturation effect in action potential trains. However, there was a qualitative difference in their effects on the shape of the transient. Incubation with the fast buffer BAPTA prolonged the decay to baseline. In contrast, the slow buffer EGTA (or EDTA) produced an initial decay faster than the control condition while also producing the slower subsequent phase observed with BAPTA. We demonstrate that these results are consistent with numerical simulations of Ca2+ dynamics in a single-compartment model where the fast initial decay is produced by the forward rate of Ca2+ binding to EGTA. 5. Ca2+ influx into tectal presynaptic structures, and also into unmyelinated axons in the isolated optic nerve, was diminished (60-70%) in the presence of the voltage-activated Ca2+ channel blocker omega-conotoxin GVIA, but was only weakly affected (approximately 10%) by omega-agatoxin IVA. 6. After 10- to 50-Hz stimulus trains, synaptic enhancement of unmyelinated fibers decayed with a characteristic time similar to fura-2 fluorescence decays. Incubation with EDTA-AM or EGTA-AM produced little effect on evoked release but reduced both the amplitude of the fura-2-measured Ca2+ transient and the amplitude of short-term synaptic enhancement.