• Journal of the Korea Convergence Society
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• v.9 no.4
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• pp.161-167
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• 2018

The amount of CNG was measured using a pressure sensor in the case of CNG vehicles. However, the current measurement method causes anxiety to the driver because it is difficult to measure the detailed amount of CNG according to various environmental conditions. This study was performed to measure the amount of CNG in CNG fuel system, and presented the method of measurement by simulating the detection system of CNG. In this experiment, a detection simulator with an ultrasonic sensor in CNG tank of Type-3 was designed, and the reception signal of the ultrasonic sensor was verified by reducing the pressure from 100 bars to 0 bars (increment=5 bars) using compressed air. As a result, the output signal voltage of the ultrasonic sensor decreased as the pressure in the tank decreased, and the it was verified that the shape of the graph was linearity.

• Journal of Preventive Medicine and Public Health
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• v.32 no.4
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• pp.459-466
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• 1999

Objectives:eurotoxicity is mediated by nitric oxide(NO) in the rat primary neuronal cultures and assess the effect of $Mn^{2+}$ on the N-methyl-D aspartate(NMDA) receptors. Methods: We have used 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT)assay to examine the effect of cytotoxicity of $MnCl_2$ in neuronal cells , NO production was determined by measuring nirites, a stable oxidation product of NO. The neurons in the rat that contains neuronal nitric oxide synthase(nNOS) were examined by immunofluorescence and confocal microscopy. The effects of $Mn^{2+}$ on the NMDA receptors was assesed by the whole cell voltage clamp technique. Results: We showed that the NO release and NOS expression was increased with 500uM $MnCl_2$ treatment and an NOS inhibitors, $N^G-nitro-L-arginine$, prevented neurotoxicity elicited by manganese. In the electrophysiological study, $Mn^{2+}$ does not block or activate the NMDA receptors and not pass through the NMDA receptors in a neurons of basal ganglia. Conclusions: It is concluded that manganese neurotoxicity in basal ganglia was partially mediated by nitric oxide in the cell culture model.

• Journal of Chest Surgery
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• v.22 no.4
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• pp.548-561
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• 1989

In single atrial cells isolated from the rabbit the properties of inward current of Na-Ca exchange were investigated using the whole cell voltage clamp technique. The current was recorded during repolarization following brief 2 ms depolarizing pulse to +40 mV from a holding potential of * 70 mV. Followings are the results obtained: 1. When stimulated every 30 seconds, the inward currents were activated and reached peak values 6-12 ms after the beginning of depolarizing pulse. The mean current amplitude was 342 pA/cell. 2. The current decayed spontaneously from the peak activation and the time course of the relaxation showed two different phases fast and slow phase. The time constants were 10-18 ms and 60-140 ms, respectively. 3. The recovery of inward current was tested by paired pulse of various intervals. The peak current recovered exponentially with time constant of 140 ms and 1 p M isoprenaline accelerated the recovery process. 4. Relaxation time course was also affected by pulse interval and time constant of the fast phase was reduced almost linearly according to the decrease of pulse interval between 30 sec and 1 sec. 5. The peak activation was increased in magnitude by long prepulse stimulation, 5 p M Bay K, 1 p M isoprenaline or internal and external application of c-AMP. 6. The relaxation time constant of the fast phase was prolonged by 5 p M Bay K or c-AMP, and shortened by isoprenaline. However the time course of the slow relaxation phase was not so much changed. From the above results, it could be concluded that increase of the calcium current by Bay K or c-AMP results in the potentiation and prolongation of intracellular calcium transient, and the facilitation of Ca uptake by SR might be a mechanism of shortening the time constant of current relaxation by short interval stimulation or isoprenaline.

• Transactions on Electrical and Electronic Materials
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• v.12 no.5
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• pp.213-217
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• 2011

The nonlinear electrical properties and degradation behavior against an impulse-current of 400 A in the ZnO-$Pr_6O_{11}$-CoO-$Cr_2O_3$-$Y_2O_3$-$Er_2O_3$ (ZPCCYE) varistors were investigated with different $Y_2O_3/Er_2O_3$ ratios. The $Y_2O_3/Er_2O_3$ mole ratio has a significant effect on nonlinear electrical properties and impulse degradation behavior of the ZPCCYE varistors. The varistors added with $Y_2O_3/Er_2O_3$ = 0.5/0.5 exhibited the best nonlinear properties with 39 in nonlinear coefficient (${\alpha}$) and the best clamp characteristics, in which the clamping voltage ratio (K) was in the range of K = 1.62-2.18 at an impulse-current of 1-50 A. The varistors added with $Y_2O_3/Er_2O_3$ = 0.25/0.5 exhibited the best electrical stability, with $%{\Delta}E_{1mA/cm^2}$=-5.6%, $%{\Delta}{\alpha}$ = 6.7%, and $%{\Delta}J_L$ = -14.6% against an impulse-current of 400 A. On the contrary, the varistors added with $Y_2O_3/Er_2O_3$ = 0.5/0.5 were destroyed applying an impulse-current of 400 A.

• The Korean Journal of Physiology and Pharmacology
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• v.3 no.6
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• pp.623-630
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• 1999

Decreased cardiac contractility occurs in endotoxicosis, but little is known about the ionic mechanism responsible for myocardial dysfunction. In this study, we examined the changes in $Ca{2+}$ and $K^+$ currents in cardiac myocytes from endotoxin-treated rat. Ventricular myocytes were isolated from normal and endotoxemic rats (ex vivo), that were treated for 10 hours with Salmonella enteritidis lipopolysaccharides (LPS; 1.5 mg/kg) intravenously. Normal cardiac myocytes were also incubated for 6 hours with 200 ng/ml LPS (in vitro). L-type $Ca{2+}$ current $(I_{Ca,L})$ and transient outward $K^+$ current $(I_{to})$ were measured using whole cell patch clamp techniques. Peak $I_{Ca,L}$ was reduced in endotoxemic myocytes (ex vivo; 6.00.4 pA/pF, P＜0.01) compared to normal myocytes (control; 10.90.6 pA/pF). Exposure to endotoxin in vitro also attenuated $I_{Ca,L}$ (8.40.4 pA/pF, P＜0.01). The amplitude of $(I_{to})$ on depolarization to 60 mV was reduced in endotoxin treated myocytes (16.51.5 pA/pF, P＜0.01, ex vivo; 20.00.9 pA/pF, P＜0.01 , in vitro) compared to normal myocytes (control; 24.71.0 pA/pF). There was no voltage shift in steady-state inactivation of $I_{Ca,L}$ and $(I_{to})$ between groups. These results suggest that endotoxin reduces $Ca{2+}$ and $K^+$ currents of rat cardiac myocytes, which may lead to cardiac dysfunction.

• The Korean Journal of Physiology and Pharmacology
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• v.8 no.3
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• pp.161-165
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• 2004

Exogenous carbon monoxide (0.2%) increases L-type calcium $(Ca^{2+})$ current in human jejunal circular smooth muscle cells. The stimulatory effect of carbon monoxide (CO) on L-type $Ca^{2+}$ current is inhibited by pre-application of L-NNA, a classical competitive inhibitor of nitric oxide synthase (NOS) with no significant isoform selectivity (Lim, 2003). In the present study, we investigated which isoform of NOS affected CO induced stimulation of L-type $Ca^{2+}$ current in human jejunal circular smooth muscle cells. Cells were voltage clamped by whole-cell mode patch clamp technique, and membrane currents were recorded with 10 mM barium as the charge carrier. Before the addition of CO, cells were pretreated with each inhibitor of three NOS isoforms for 15 minutes. CO-stimulating effect on L-type $Ca^{2+}$ current was partially blocked by N-(3-(Amino-methyl) benzyl) acetamidine 2HCl (1400W, an iNOS inhibitor). On the other hand, 3-bromo-7-nitroindazole (BNI, a nNOS inhibitor) or $N^5-(1-Iminoethyl)-L-ornithine$ dihydrochloride (L-NIO, an eNOS inhibitor) completely blocked the CO effect. These data suggest that low dose of exogenous CO may stimulate all NOS isoforms to increase L-type $Ca^{2+}$ channel through nitric oxide (NO) pathway in human jejunal circular smooth muscle cells.

• The Korean Journal of Physiology and Pharmacology
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• v.17 no.5
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• pp.463-468
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• 2013

Acute hypoxia induces contraction of pulmonary artery (PA) to protect ventilation/perfusion mismatch in lungs. As for the cellular mechanism of hypoxic pulmonary vasoconstriction (HPV), hypoxic inhibition of voltage-gated $K^+$ channel (Kv) in PA smooth muscle cell (PASMC) has been suggested. In addition, our recent study showed that thromboxane $A_2$ ($TXA_2$) and hypoxia-activated nonselective cation channel ($I_{NSC}$) is also essential for HPV. However, it is not well understood whether HPV is maintained in the animals exposed to ambient hypoxia for two days (2d-H). Specifically, the associated electrophysiological changes in PASMCs have not been studied. Here we investigate the effects of 2d-H on HPV in isolated ventilated/perfused lungs (V/P lungs) from rats. HPV was almost abolished without structural remodeling of PA in 2d-H rats, and the lost HPV was not recovered by Kv inhibitor, 4-aminopyridine. Patch clamp study showed that the hypoxic inhibition of Kv current in PASMC was similar between 2d-H and control. In contrast, hypoxia and $TXA_2$-activated $I_{NSC}$ was not observed in PASMCs of 2d-H. From above results, it is suggested that the decreased $I_{NSC}$ might be the primary functional cause of HPV disappearance in the relatively early period (2 d) of hypoxia.

• The Korean Journal of Physiology and Pharmacology
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• v.16 no.5
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• pp.327-332
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• 2012

Sertraline is a commonly used antidepressant of the selective serotonin reuptake inhibitors (SSRIs) class. In these experiments, we have used the whole cell patch clamp technique to examine the effects of sertraline on the major cardiac ion channels expressed in HEK293 cells and the native voltage-gated $Ca^{2+}$ channels in rat ventricular myocytes. According to the results, sertraline is a potent blocker of cardiac $K^+$ channels, such as hERG, $I_{Ks}$ and $I_{K1}$. The rank order of inhibitory potency was hERG > $I_{K1}$ > $I_{Ks}$ with $IC_{50}$ values of 0.7, 10.5, and 15.2 ${\mu}M$, respectively. In addition to $K^+$ channels, sertraline also inhibited $I_{Na}$ and $I_{Ca}$, and the $IC_{50}$ values are 6.1 and 2.6 ${\mu}M$, respectively. Modification of these ion channels by sertraline could induce changes of the cardiac action potential duration and QT interval, and might result in cardiac arrhythmia.

• The Korean Journal of Physiology and Pharmacology
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• v.16 no.2
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• pp.113-118
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• 2012

Ginsenosides are low molecular weight glycosides found in ginseng that exhibit neuroprotective effects through inhibition of $N$-methyl-D-aspartic acid (NMDA) receptor channel activity. Ginsenosides, like other natural compounds, are metabolized by gastric juices and intestinal microorganisms to produce ginsenoside metabolites. However, little is known about how ginsenoside metabolites regulate NMDA receptor channel activity. In the present study, we investigated the effects of ginsenoside metabolites, such as compound K (CK), protopanaxadiol (PPD), and protopanaxatriol (PPT), on oocytes that heterologously express the rat NMDA receptor. NMDA receptor-mediated ion current ($I_{NMDA}$) was measured using the 2-electrode voltage clamp technique. In oocytes injected with cRNAs encoding NMDA receptor subunits, PPT, but not CK or PPD, reversibly inhibited $I_{NMDA}$ in a concentration-dependent manner. The $IC_{50}$ for PPT on $I_{NMDA}$ was $48.1{\pm}4.6\;{\mu}M$, was non-competitive with NMDA, and was independent of the membrane holding potential. These results demonstrate the possibility that PPT interacts with the NMDA receptor, although not at the NMDA binding site, and that the inhibitory effects of PPT on $I_{NMDA}$ could be related to ginseng-mediated neuroprotection.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.5
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• pp.611-616
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• 1998

Although the $Ca^{2+}-activated\;K^+\;(I_{K,Ca})$ channel is known to play an important role in the maintenance of resting membrane potential, the regulation of the channel in physiological condition is not completely understood in vascular myocytes. In this study, we investigated the role of cytoplasmic $Mg^{2+}$ on the regulation of $I_{K,Ca}$ channel in pulmonary arterial myocytes of the rabbit using the inside-out patch clamp technique. $Mg^{2+}$ increased open probability (Po), but decreased the magnitude of single channel current. $Mg^{2+}-induced$ block of unitary current showed strong voltage dependence but increase of Po by $Mg^{2+}$ was not dependent on the membrane potential. The apparent effect of $Mg^{2+}$ might, thus, depend on the proportion between opposite effects on the Po and on the conductance of $I_{K,Ca}$ channel. In low concentration of cytoplasmic $Ca^{2+},\;Mg^{2+}$ increased $I_{K,Ca}$ by mainly enhancement of Po. However, at very high concentration of cytoplasmic $Ca^{2+},$ such as pCa 5.5, $Mg^{2+}$ decreased $I_{K,Ca}$ through the inhibition of unitary current. Moreover, $Mg^{2+}$ could activate the channel even in the absence of $Ca^{2+}.\;Mg^{2+}$ might, therefore, partly contribute to the opening of $I_{K,Ca}$ channel in resting membrane potential. This phenomenon might explain why $I_{K,Ca}$ contributes to the resting membrane potential where membrane potential and concentration of free $Ca^{2+}$ are very low.