• Archives of Pharmacal Research
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• v.8 no.2
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• pp.49-57
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• 1985

The effect of ginseng components on the potassium depleted cardiomyopathic rat heart was investigated. In the perfused heart experiment using Langendorff apparatus, the deterioration rate of contriactile force of potassium depleted rat heart (low potassium diet group) was faster than that of normal rat heart and ginseng components showed the ability to slow the deterioration rate of potassium depleted hearts. Both sialic acid contents in carcolemmal ghost and sialyltransferase activity of 40,000 * g subcellular fraction prepared from cardiac ventricular tissue of low potassium diet group were significantly decreased compared to those of normal group. The decrease of the sialic acid content and sialyltransferase activity in sarcolemma of low potassium diet group was inhibited when ginseng was concomitantly administered. Calcium uptake of sarcoplasmic reticulum prepared from low potassium diet group was significantly greaterthan that of normal group. Ginseng extract or total saponin showed the tendency to inhibit the increase of cacium uptake.

• The Korean Journal of Physiology
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• v.14 no.1
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• pp.31-39
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• 1980

Changes in cardiac performances were observed under variations of the arterial and/or venous pressures with K-loading or K-depletion in turtle heart. Hearts were perfused with turtle Ringer-Locke's solutions containing various levels of potassium ion concentration. When venous pressure increased from 4 to 12 cm $H_2O$, cardiac output increased from $6.2{\pm}0.68$ to $15.7{\pm}0.75\;ml/min$, concomittantly. On the contrary, cardiac output decreased during the elevation of arterial pressure. Stroke work increased more prominently during the arterial pressure elevation than during the elevation of venous pressure. During K-depletion$(1{\sim}2mEq/L)$, cardiac output increased to two times that of normal K-concentration$(3{\sim}6\;mEq/L)$ group. Heart rate increased also, but less markedly. In K-loaded$(7{\sim}8\;mEq/L)$ group, both the cardiac output and heart rate decreased but stroke volume rather increased, because heart rate decrement was disproportionate to that of cardiac output. We concluded that in perfused turtle heart, cardiac output variation was more sensitive to K_depletion whereas heart rate to K-loading.

• The Korean Journal of Physiology and Pharmacology
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• v.13 no.1
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• pp.15-22
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• 2009

This study was undertaken to elucidate the underlying mechanisms of ATP depletion-induced membrane transport dysfunction and cell death in renal proximal tubular cells. ATP depletion was induced by incubating cells with 2.5 mM potassium cyanide(KCN)/0.1 mM iodoacetic acid(IAA), and membrane transport function and cell viability were evaluated by measuring $Na^+$-dependent phosphate uptake and trypan blue exclusion, respectively. ATP depletion resulted in a decrease in $Na^+$-dependent phosphate uptake and cell viability in a time-dependent manner. ATP depletion inhibited $Na^+$-dependent phosphate uptake in cells, when treated with 2 mM ouabain, a $Na^+$ pump-specific inhibitor, suggesting that ATP depletion impairs membrane transport functional integrity. Alterations in $Na^+$-dependent phosphate uptake and cell viability induced by ATP depletion were prevented by the hydrogen peroxide scavenger such as catalase and the hydroxyl radical scavengers(dimethylthiourea and thiourea), and amino acids(glycine and alanine). ATP depletion caused arachidonic acid release and increased mRNA levels of cytosolic phospholipase $A_2(cPLA_2)$. The ATP depletion-dependent arachidonic acid release was inhibited by $cPLA_2$ specific inhibitor $AACOCF_3$. ATP depletion-induced alterations in $Na^+$-dependent phosphate uptake and cell viability were prevented by $AACOCF_3$. Inhibition of $Na^+$-dependent phosphate uptake by ATP depletion was prevented by antipain and leupetin, serine/cysteine protease inhibitors, whereas ATP depletion-induced cell death was not altered by these agents. These results indicate that ATP depletion-induced alterations in membrane transport function and cell viability are due to reactive oxygen species generation and $cPLA_2$ activation in renal proximal tubular cells. In addition, the present data suggest that serine/cysteine proteases play an important role in membrane transport dysfunction, but not cell death, induced by ATP depletion.

• The Korean Journal of Physiology
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• v.10 no.2
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• pp.29-37
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• 1976

Effect of furosemide administration on glucose tolerance, insulin-and HGH response following parenteral glucose loading was studied in healthy subjects. Effects of potassium or calcium on the furosemide induced changes were also observed in the same subjects. Furosemide administration resulted in a considerable reduction in the magnitude and duration of insulin response although no obvious changes were observed in glucose disappearance from the circulation. Oral potassium or calcium supplement to the furosemide treated subjects showed a reversion toward normal of the insulin response. The author suggested that a decreased endogenous insulin production resulting from the potassium and/or calcium depletion is responsible for the changes observed. In those subjects who receive parenteral nutrition if administration of furosemide is essential, it should be supplemented by potassium and/or calcium.

• BMB Reports
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• v.32 no.3
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• pp.273-278
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• 1999

Cytolysin produced by Vibrio vulnificus has been known to be lethal to mice by increasing vascular permeability and neutrophil sequestration in the lung. In the present study, a cytotoxic mechanism of V. vulnificus cytolysin on the neutrophil was investigated. Cytolysin rapidly bound to neutrophils and induced cell death, as determined by the trypan blue exclusion test. V. vulnificus cytolysin caused the depletion of cellular ATP without the release of ATP or lactate dehydrogenase. Formation of transmembrane pores was evidenced by the rapid efflux of potassium and 2-deoxy-D-[$^3H$]glucose from cytolysin-treated neutrophils. It was further confirmed by the rapid flow of monovalent ions in the patch clamp of cytolysin-treated neutrophil membrane. The pore formation was accompanied by the oligomerization of cytolysin monomers on the neutrophil membrane as demonstrated by immunoblot, which exhibited a 210 kDa band corresponding to a tetramer of the native cytolysin of $M_r$ 51,000. These findings indicate that V. vulnificus cytolysin rapidly binds to the neutrophil membrane and oligomerizes to form small transmembrane pores, which induce the efflux of potassium and the depletion of cellular ATP leading to cell death without cytolysis.

• IMMUNE NETWORK
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• v.12 no.6
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• pp.284-290
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• 2012

Innate immune cells sense and respond to the cytoplasmic infection of bacterial pathogens through NLRP3, NLRC4 or AIM2 inflammasome depending on the unique molecular pattern of invading pathogens. The infection of flagellin- or type III secretion system (T3SS)-containing Gram-negative bacteria such as Salmonella enterica serovar Typhimurium (S. typhimurium) or Pseudomonas aeruginosa (P. aeruginosa) triggers NLRC4-dependent caspase-1 activation leading to the secretion of proinflammatory cytokines such as interleukin-1-beta (IL-$1{\beta}$) and IL-18. Previous studies have shown that apoptosis-associated speck-like protein containing a CARD (ASC) is also required for Salmonella-induced caspase-1 activation, but it is still unclear how ASC contributes to the activation of NLRC4 inflammasome in response to S. typhimurium infection. In this study, we demonstrate that S. typhimurium triggers the formation of ASC oligomer in a potassium depletion-independent manner as determined by in vitro crosslinking and in situ fluorescence imaging. Remarkably, inhibition of potassium efflux failed to block Salmonella-promoted caspase-1 activation and macrophage cell death. These results collectively suggest that ASC is substantially oligomerized to facilitate the activation of caspase-1 in response to S. typhimurium infection. Contrary to NLRP3 inflammasome, intracellular potassium depletion is not critical for NLRC4 inflammasome signaling by S. typhimurium.

• The Korean Journal of Physiology
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• v.9 no.2
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• pp.33-39
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• 1975

Changes of urinary aldosterone excretion, concurrent sodium and potassium excretion following furosemide administration were studied in normotensive young Korean with high sodium intake, moderate sodium restriction and marked sodium depletion. After intravenous injection of furosemd 40mg, plasma and urine samples were collected at every thirty minutes for two hours. Plasma-and urinary aldosterone, electrolyte concentration and urine flow rate were measured by means of radioimmunoassay or flamephotometry. Relations of urinary aldosterone to concurrent sodium or potassium/sodium ratio, and of urinary aldosterone to concurrent plasma aldosterone activity were studied. Following were the results: 1. Furosemide administration resulted in a increased urinary aldosterone concentration and unchanged or somewhat decreased sodium concentration in course of time after the injection. 2. Urinary potassium concentration showed initial decrease and subsequent increase in course of time after furosemide administration and it resulted in a gradual increase in urinary potassium/sodium ratio. 3. Studying the relations between urinary aldosterone excretion and potassium/sodium excretion ratio, or sodium excretion were meaningless because of the urinary flow rate after the injection was decreased with time course. 4. Furosemide administration showed a good relationship of urinary aldosterone concentration to concurrent potassium/sodium ratio rather than concurrent sodium concentration in subjects with sodium restriction, but no meaningful relationship was detected in subjects with high sodium intake because increasing rate of the ratio was not so wide. 5. Furosemide also resulted a reasonable relation of plasma aldosterone concentration to concurrent urinary aldosterone concentration especially during low sodium intake. 6. Above results suggested that relation of urinary aldosterone concentration to K/Na ratio following furosemide administration during sodium restriction is significant and has a benefit to reduce the variation induced by kalemic change showing in the diragram for daily aldosterone to sodium excretion.

• Proceedings of the Korean Institute of Electrical and Electronic Material Engineers Conference
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• 1995.05a
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• pp.73-76
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• 1995

In this study, the slab waveguide was fabricated using potassium-nitride(KNO$_3$) or silver-nitride (AgNO$_3$) molten sources by ion-exchange process. The effective refractive indices of waveguide were measured by Prism-Coupling method. and The characteristics of waveguide(mode dispersion, effective diffusion depth. surface refractive index, diffusion coefficient, and refractive index profile etc,) were investigated by WKB method, In the case of potassium ion-exchange, the computer calculation showed that the refractive index profile of waveguide followed Gaussian function, the surface refractive index increased with ion-exchange time and the effective diffusion depth increased a little as ion-exchange time increased, while the surface refractive index of silver ion-exchanged waveguide decreased with ion-exchange time because of the ion depletion on the surface of waveguide, and the effective diffusion depth seriously with ion-exchange tim. Double ion-exchanged waveguide was fabricated by performing silver ion-exchange after potassium ion-exchange. Double ion-exchanged waveguide had a tight mode binding force since the surface refractive index was larger than single step ion-exchanged waveguide.

• Korean Journal of Veterinary Research
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• v.40 no.2
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• pp.267-274
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• 2000

Since intracellular free $Mg^{2+}$ ($[Mg^{2+}]_i$) appears to be tightly regulated following cellular energy depletion, we hypothesized that the increase in $[Mg^{2+}]_i$ would result in $Mg^{2+}$ extrusion into circulation. Extracellualr $Mg^{2+}$ contents ($[Mg^{2+}]_o$) were measured in rat erythrocytes, the perfused heart and liver, and plasma in the anesthetized rat. Animals were injected intraperitoneally with sodium nitrite ($NaNO_2$) and plasma $Mg^{2+}$ was measured after the injection and then 10 and 20 minutes later. An increase in circulating (plasma) $Mg^{2+}$ ($[Mg^{2+}]_c$) and methemoglobin was observed in animals injected with $NaNO_2$ (30 mg/Kg). The time course of the effects demonstrated that $[Mg^{2+}]_c$ and methemoglobin continued to increase 10 minutes after the $NaNO_2$ injection. Under these conditions, there was a sustained increase in $[Mg^{2+}]_c$, but not in methemoglobin, which was inhibited by pretreatment with potassium cyanide (KCN, 4 mg/Kg), indicating that an increase in $[Mg^{2+}]_c$ was accompanied by ATP depletion. Injection of rotenone (0.9 mg/Kg) or 2,4-dinitrophenol (15 mg/Kg) also induced an increase in $[Mg^{2+}]_c$. Reduced respiration rate from 100/min to 10/min during 30 minutes also caused a time-dependent rise in $[Mg^{2+}]_c$. These increase in $[Mg^{2+}]_c$ were inhibited by pretreatment with KCN. In addition, ATP depletion by $NaNO_2$ or KCN sustainedly increased the $[Mg^{2+}]_o$ in rat erythrocytes. $Mg^{2+}$ efflux was stimulated by KCN in the perfused heart and liver, but not by $NaNO_2$. These results suggest that the activation of $Mg^{2+}$ effluxes into the circulation is directly dependent on the ATP depletion-induced increase in $[Mg^{2+}]_i$ and heart, liver and erythrocytes have a major pool of $Mg^{2+}$ that can be mobilized upon cellular energy state.

• Nuclear Engineering and Technology
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• v.51 no.3
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• pp.755-760
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• 2019

Compound samples based on the mineral-like magnesium potassium phosphate matrix $MgKPO_4{\times}6H_2O$ were synthesized by solidification of high level waste surrogate. Phase composition and structure of synthesized samples were studied by XRD and SEM methods. Compressive strength of the compounds is $12{\pm}3MPa$. Coefficient of thermal expansion of the samples in the range $250-550^{\circ}C$ is $(11.6{\pm}0.3){\times}10^{-6}1/^{\circ}C$, and coefficient of thermal conductivity in the range $20-500^{\circ}C$ is $0.5W/(m{\times}K)$. Differential leaching rate of elements from the compound, $g/(cm^2{\times}day)$: $Mg-6.7{\times}10^{-6}$, $K-3.0{\times}10^{-4}$, $P-1.2{\times}10^{-4}$, $^{137}Cs-4.6{\times}10^{-7}$; $^{90}Sr-9.6{\times}10^{-7}$; $^{239}Pu-3.7{\times}10^{-9}$, $^{241}Am-9.6{\times}10^{-10}$. Leaching mechanism of radionuclides from the samples at the first 1-2 weeks of the leaching test is determined by dissolution ($^{137}Cs$), wash off ($^{90}Sr$) or diffusion ($^{239}Pu$ and $^{241}Am$) from the compound surface, and when the tests continue to 90-91 days - by surface layer depletion of compound. Since the composition and physico-chemical properties of the compound after irradiation with an electron beam (absorbed dose of 1 MGy) are constant the radiation resistance of compound was established.