Academic literature on the topic 'Hypotonic shock'
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Journal articles on the topic "Hypotonic shock"
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Dinh, Xuan Tu, Huynh Thi Diem Suong Le, and Minh Ly Nguyen. "The chromosome numbers of Panax vietnamensis Ha et Grushv." Can Tho University Journal of Science 14, CBA (October 27, 2022): 86–90. http://dx.doi.org/10.22144/ctu.jen.2022.033.
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The somatic chromosome number of Panax vietnamensis Ha et Grushv. was determined to be 2n = 24, based on the hypotonic shock method by potassium chloride solution. In this study, we investigated the effect of potassium chloride and colchicine solutions on chromosome dispersion of Panax vietnamensis at different concentrations. The treatment using 0.2% KCl solution in 45 minutes combined with 0.05% colchicine solution in 2 hours subsequently resulted in proper hypotonia. The result showed that chromosomes were evenly dispersed. The hypotonic shock method seemed to be effective in equally distributing chromosomes. The result can be applied in cell genetic studies and selective breeding programs for Panax vietnamensis.
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Beck, J. S., S. Breton, G. Giebisch, and R. Laprade. "Potassium conductance regulation by pH during volume regulation in rabbit proximal convoluted tubules." American Journal of Physiology-Renal Physiology 263, no. 3 (September 1, 1992): F453—F458. http://dx.doi.org/10.1152/ajprenal.1992.263.3.f453.
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When rabbit proximal convoluted tubules were microperfused in the presence of bicarbonate, a 90 mosmol hypotonic shock hyperpolarized the basolateral membrane by 5.5 +/- 1.4 mV, increased basolateral potassium selectivity (tK) from 0.30 +/- 0.02 to 0.45 +/- 0.02, and reduced the basolateral membrane resistance from 4,887 +/- 821 to 2,836 +/- 602 omega.cm. These data show that the hypotonic shock increased absolute basolateral potassium conductance. The same hypotonic shock elevated intracellular pH from 7.18 +/- 0.04 to 7.31 +/- 0.04. When bath pH was increased by 0.2 pH units (by reduction of CO2), intracellular pH rose by 0.13 +/- 0.01. In separate experiments this maneuver hyperpolarized the basolateral membrane by 5.0 +/- 0.8 mV and augmented basolateral tK from 0.58 +/- 0.06 to 0.68 +/- 0.04, suggesting that the basolateral potassium conductance is sensitive to pH changes of a magnitude similar to that evoked by a hypotonic shock. In the nominal absence of bicarbonate or presence of 0.5 mM 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid (SITS) in the bath, the hypotonic shock caused a transient intracellular acidification, suggesting involvement of basolateral bicarbonate transport in the hypotonic shock-induced alkalinization. In the absence of bicarbonate, the hypotonic shock did not increase basolateral tK or induce hyperpolarization of the basolateral membrane. We conclude that the increase in potassium conductance observed during hypotonic shock is at least partly mediated by a bicarbonate-dependent, SITS-sensitive intracellular alkalinization.
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Marshall, W. S., S. E. Bryson, and T. Luby. "Control of epithelial Cl(−) secretion by basolateral osmolality in the euryhaline teleost Fundulus heteroclitus." Journal of Experimental Biology 203, no. 12 (June 15, 2000): 1897–905. http://dx.doi.org/10.1242/jeb.203.12.1897.
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Euryhaline teleost fish adapt rapidly to salinity change and reduce their rate of ion secretion on entry to fresh water. Killifish (Fundulus heteroclitus) transferred from full-strength sea water to fresh water showed large reductions in plasma [Na(+)] and osmolality at 6 h which were corrected by 24 h. To mimic this in vitro, a hypotonic shock of 20–70 mosmol kg(−)(1) was applied on the basolateral side of opercular epithelia. This hypotonic shock reversibly reduced the short-circuit current (I(sc), equivalent to the rate of secretion of Cl(−)) in a dose-dependent fashion, with a 40 mosmol kg(−)(1) hypotonic shock reducing I(sc) by 58+/−4.6 % in 40 min. Similar reductions in [NaCl], but with added mannitol to maintain osmolality, were without effect, indicating that the effect was purely osmotic. Hypotonic inhibition of I(sc) was accompanied by reductions in epithelial conductance (G(t)) but no significant change in transepithelial potential (V(t)). The hypotonic inhibition was apparently not Ca(2+)-mediated because Ca(2+)-depleted salines, thapsigargin and ionomycin all failed to block the reduction in I(sc) produced by hypotonic shock. The inhibition was not mediated via a reduction in intracellular cyclic AMP level because cyclic AMP levels, measured by radioimmunoassay, were unchanged by hypotonic shock and by 1.0 micromol l(−)(1) clonidine (which inhibits I(sc) by changing intracellular [Ca(2+)]) but were increased markedly by 1.0 micromol l(−)(1) isoproterenol, a positive control. The protein tyrosine kinase inhibitor genistein (100 micromol l(−)(1)), but not its inactive analogue daidzein, inhibited I(sc) in normal osmolality but produced a stimulation of I(sc) after hypotonic shock (and after clonidine treatment). The inhibitory effects of genistein and hypotonicity were not additive, suggesting that the same portion of the I(sc) was inhibited by both treatments. These data are consistent with a model for Cl(−) transport regulation involving tyrosine phosphorylation in cell-swelling-induced inhibition of Cl(−) secretion when euryhaline teleosts adapt to fresh water.
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Bear, C. E. "A nonselective cation channel in rat liver cells is activated by membrane stretch." American Journal of Physiology-Cell Physiology 258, no. 3 (March 1, 1990): C421—C428. http://dx.doi.org/10.1152/ajpcell.1990.258.3.c421.
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A 16-pS channel was studied using patch-clamp electrophysiology in freshly dissociated rat liver cells and rat hepatoma cells. The channel was found to be cation selective and permeable to Na+, K+, and Ca2+. Its gating was unaffected by addition of the calcium ionophore A23187 (5 microM) in the presence of extracellular Ca2+ (2 mM). Ca2+ channel blockers, nifedipine, verapamil, and lanthanum, failed to inhibit the channel. The channel was activated by stretch, applied as suction to the interior of the patch pipette, and by cell swelling, induced by hypotonic shock or organic solute uptake (10 mM L-alanine). Channel activation by cell swelling was transient, lasting approximately 1 min. An elevation in cytosolic Ca2+ was evoked by hypotonic shock, as measured using the fluorescent indicator indo-1/AM. This change in intracellular Ca2+ concentration was dependent on extracellular Ca2+. Inasmuch as the time course for this response corresponded to that of channel activation, it is likely that hypotonic shock stimulated Ca2+ influx through the stretch-activated channel. To determine the role for Ca2+ influx in regulatory volume decrease (RVD), cell volume changes after hypotonic shock were studied using a Coulter counter. RVD was slightly but significantly inhibited by depletion of extracellular Ca2+. On the basis of these results it is proposed that stretch-activated channels in liver cells permit the transient influx of Ca2+, which in turn acts to trigger changes in ion conductance or cytoskeletal components involved in cell volume regulation.
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Fujii, Shuhei, and Johan A. Hellebust. "Release of intracellular glycerol and pore formation in Dunaliella tertiolecta exposed to hypotonic stress." Canadian Journal of Botany 70, no. 7 (July 1, 1992): 1313–18. http://dx.doi.org/10.1139/b92-164.
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When Dunaliella tertiolecta cells, previously cultured in a 0.5 M NaCl medium, were resuspended in a 0.25 NaCl medium, about 50% of the intracellular glycerol was lost within 2 min. A corresponding amount of glycerol appeared in the medium, while other organic solutes, such as amino acids and sugars, were not detected. These results indicate that intracellular glycerol is rapidly released without significant concomitant cell damage. Rubidum, in the case of rubidium-loaded cells, was also rapidly released to the medium in response to hypotonic shock. Gramicidin, dimers of which form stable membrane pores, caused rapid release of intracellular glycerol, while the ionophore, valinomycin, had no effect. When 0.5 M NaCl-grown cells were resuspended in 0.25 M NaCl medium, intracellular trapping of 14C-glycerol occurred but not of 14C-glucose, 14C-sucrose, or 14C-glycine. However, when 0.5 M NaCl-grown cells were resuspended in 0.05 M NaCl medium, intracellular trapping of small amounts of, 14C-glucose, 14C-sucrose, or 14C-glycine, in addition to considerable amounts of 14C-glycerol, occurred. These results indicate that abrupt hypotonic shocks cause transient formation of small nonspecific pores in the plasma membrane of D. tertiolecta cells and that intracellular glycerol is released to the medium through such nonspecific transient pores. Key words: Dunaliella, hypotonic shock, glycerol release, rubidum, pore formation.
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Macri, P., S. Breton, J. S. Beck, J. Cardinal, and R. Laprade. "Basolateral K+, Cl-, and HCO3- conductances and cell volume regulation in rabbit PCT." American Journal of Physiology-Renal Physiology 264, no. 2 (February 1, 1993): F365—F376. http://dx.doi.org/10.1152/ajprenal.1993.264.2.f365.
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The relationship between changes in cellular volume, intracellular pH (pHi), basolateral membrane potential (VBL), and membrane partial basolateral conductances to K+ (tK) and Cl- (tCl) and mediated by the Na-HCO3 cotransporter (tNaHCO3) was determined in the collapsed proximal convoluted tubule (PCT) submitted to a 125-mosmol/kg hypotonic shock. The shock that produces a rapid swelling followed by partial volume regulation was accompanied by a rapid and transient VBL hyperpolarization of 10.0 +/- 1.5 mV and a second gradual hyperpolarization of 5.0 +/- 0.7 mV with respect to a control value of -44.0 +/- 4.6 mV.tK was 0.12 +/- 0.03 in control, increased transiently to 0.15 +/- 0.03, and then gradually increased to reach 0.32 +/- 0.06 at the end of hypotonic shock. In contrast, tCl was 0.03 +/- 0.01 in control, increased rapidly to a maximum of 0.16 +/- 0.01, and then decreased slowly to 0.08 +/- 0.02. During the same period, tNaHCO3 decreased rapidly from 0.41 +/- 0.04 to a minimum of 0.11 +/- 0.02 and slowly reincreased to reach 0.16 +/- 0.01.pHi increased transiently from 7.09 +/- 0.03 in control to 7.24 +/- 0.05 to come back gradually to 7.15 +/- 0.05 at the end of the hypotonic period. The membrane absolute conductance mediated by the Na-HCO3 cotransporter was found to increase only slightly in hypotonic conditions, whereas that to K+ and Cl-, GK and GCl, increased by at least factors of 8 and 17, respectively, with the increase of GCl being much faster than that of GK. In addition, the temporal variations in GCl followed closely those of the cellular water efflux. We conclude that the hypotonic swelling leads to important increases in the conductive pathways for K+ and Cl- and that the Cl- conductance pathway appears to be the rate limiting step in triggering and supporting regulatory volume decrease.
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Batiza, Ann F., Tara Schulz, and Patrick H. Masson. "Yeast Respond to Hypotonic Shock with a Calcium Pulse." Journal of Biological Chemistry 271, no. 38 (September 20, 1996): 23357–62. http://dx.doi.org/10.1074/jbc.271.38.23357.
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Galietta, L. J., S. Falzoni, F. Di Virgilio, G. Romeo, and O. Zegarra-Moran. "Characterization of volume-sensitive taurine- and Cl(-)-permeable channels." American Journal of Physiology-Cell Physiology 273, no. 1 (July 1, 1997): C57—C66. http://dx.doi.org/10.1152/ajpcell.1997.273.1.c57.
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Volume-sensitive Cl- channels [ICl(vol)] were studied using taurine efflux and patch-clamp experiments in 9HTEo- human tracheal cells. Cells were stimulated with the Ca(2+)- elevating agents ATP and ionomycin in isotonic medium or in hypotonic solutions. ATP (100 microM) or ionomycin (1 microM) and hypotonic shock produced a synergic effect. Indeed, the resulting taurine efflux was much higher than the sum of the single effects elicited by ATP, ionomycin, or hypotonic medium. The taurine release elicited by hypotonic shock and the potentiation by ATP and ionomycin were markedly inhibited by using a Ca(2+)-free extracellular medium and by incubating the cells with the membrane-permeable 1,2-bis(2-amino- phenoxy)ethane-N,N,N',N'-tetraacetic acid acetoxymethyl ester chelating agent. Patch-clamp experiments confirmed the role of Ca2+ on ICl(vol) channels. Swelling-induced taurine efflux was inhibited by reactive blue 2, suramin, and pyridoxalphosphate-6-azophenyl-2',4'-disulfonic acid. Patch-clamp experiments demonstrated that these compounds shift the voltage-dependent inactivation of ICl(vol) channels toward more negative values. This study indicates that the sensitivity of ICl(vol) to cell volume changes is modulated by intracellular Ca2+ and that purinergic receptor antagonists represent a new class of CI- channel blockers.
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Smets, Ilse, Marcel Ameloot, Paul Steels, and Willy Van Driessche. "Loss of cell volume regulation during metabolic inhibition in renal epithelial cells (A6): role of intracellular pH." American Journal of Physiology-Cell Physiology 283, no. 2 (August 1, 2002): C535—C544. http://dx.doi.org/10.1152/ajpcell.00371.2001.
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In renal ischemia, tubular obstruction induced by swelling of epithelial cells might be an important mechanism for reduction of the glomerular filtration rate. We investigated ischemic cell swelling by examining volume regulation of A6 cells during metabolic inhibition (MI) induced by cyanide and 2-deoxyglucose. Changes in cell volume were monitored by recording cell thickness ( T c). Intracellular pH (pHc) measurements were performed with the pH-sensitive probe 5-chloromethyl-fluoresceine diacetate. T c measurements showed that MI increases cell volume. Cell swelling during MI is proportional to the rate of Na+ transport and is not followed by a volume regulatory response. Furthermore, MI prevents the regulatory volume decrease (RVD) elicited by a hyposmotic shock. MI induces a pronounced intracellular acidification that is conserved during a subsequent hypotonic shock. A transient acidification induced by a NH4Cl prepulse causes a marked delay of the RVD in response to a hypotonic shock. On the other hand, acute lowering of external pH to 5, simultaneously with the hypotonic shock, allowed the onset of RVD. However, this RVD was completely arrested ∼10 min after the initiation of the hyposmotic challenge. The inhibition of RVD appears to be related to the pronounced acidification that occurred within this time period. In contrast, when external pH was lowered 20 min before the hyposmotic shock, RVD was absent. These data suggest that internal acidification inhibits cellular volume regulation in A6 cells. Therefore, the intracellular acidification associated with MI might at least partly account for the failure of volume regulation in swollen epithelial cells.
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Dube, L., L. Parent, and R. Sauve. "Hypotonic shock activates a maxi K+ channel in primary cultured proximal tubule cells." American Journal of Physiology-Renal Physiology 259, no. 2 (August 1, 1990): F348—F356. http://dx.doi.org/10.1152/ajprenal.1990.259.2.f348.
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The nature and function of the ionic channels at the apical membrane of primary cultured proximal tubule cells (PT) was investigated by use of the extracellular patch-clamp method. Several types of ionic channels were observed, including a calcium-dependent K+ channel of 206 pS in symmetrical 162 mM KCl activated at depolarizing potentials [maxi K+(Ca2+)]. Whole cell experiments were also carried out that clearly indicated that the PT cells respond to a hypotonic shock by activating electroconductive pathways. This response consisted of an initial hyperpolarization (from -47 to -58 mV, SD = 3, n = 4), followed by a strong depolarization (to -23 mV, SD = 4, n = 4). Furthermore, it was found in cell-attached experiments that the maxi K+(Ca2+) channel becomes activated during the hypotonic challenge. The activation process required external Ca2+, although some residual single-channel activity was measured in the absence of extracellular calcium (n = 3). On the basis of these results, it is concluded that the volume regulation process in PT cells in response to a hypotonic shock involves an influx of calcium from the external medium, which in turn triggers the opening of apical maxi K+(Ca2+) channels.
Dissertations / Theses on the topic "Hypotonic shock"
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GROPPI, SILVIA. "Glucose and osmotic stress-dependent calcium signalling in saccharomyces cerevisiae: evidences for novel transporter systems and calcineurin involvement." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2012. http://hdl.handle.net/10281/29495.
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The major goal of this work is to understand function and regulation mechanisms of calcium transport systems in Saccharomyces cerevisiae, in response to nutrients and hypotonic shock.
Calcium represents, in fact, one of the most important second messengers in all eukaryotic cells, and particularly in budding yeast, where it plays essential roles in regulating many fundamental cellular processes, such as cell cycle, mating, sensing of glucose and glucose starvation, resistance to salt stress and cell survival.
Yeast cells actively maintain cytosolic free Ca2+ concentration at extremely low levels, in a range of 50-200 nM, through a finely regulated homeostasis maintaining mechanism.
Glucose addition to nutrient-deprived cells triggers a rapid and transient increase in cytosolic Ca2+ level, mainly due to an influx of calcium from the extracellular environment (Eilam et al., 1990). Conversely, hypotonic shock induces an increase in cytosolic Ca2+ level, mainly mediated by calcium release from intracellular stores (Batiza et al., 1996), though the intracellular transporters involved in this signalling are not yet identified.
Glucose-triggered calcium influx from extracellular environment is mediated by a high affinity calcium transporter (HACS), composed by Mid1p/Cch1p subunits, during growth in minimal medium, whereas in rich media cultured cells it seems to be mediated by a still unidentified transporter, named GIC (for Glucose Induced Calcium Channel).
By taking advantage of a bioluminescent assay in vivo allowing us to monitor cytosolic Ca2+ level changes, based on aequorin bioluminescent protein, the role of the known calcium channels and of the still unidentified putative transporters in glucose and hypotonic shock-dependent Ca2+ signalling, was here investigated.
In order to better characterize GIC and the unknown hypotonic shock-responsive intracellular transporters, a pharmacological approach was applied, testing their sensitivity to common blockers of mammalian voltage-gated calcium channels.
In addition, the effects of glucose-induced Ca2+ signalling on calcineurin, the major effector for intracellular calcium, were here investigated, demonstrating for the first time that calcineurin activation, normally recognized as being essential for survival under diverse stress conditions, can be also responsive to nutrients. The emergent role of calcineurin in regulating functionality of calcium transporters depending on nutrient availability and the crosstalk between calcineurin pathway and nutrient sensing were also investigated in this work.
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Umam, Khotibul, and 郭迪曼. "The potential osmoprotective roles of branchial heat shock proteins in milkfish upon hypotonic challenge." Thesis, 2016. http://ndltd.ncl.edu.tw/handle/47424911364428395954.
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碩士國立中興大學
生命科學院碩士在職專班
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The present study investigated the HSPs expression induced by hypotonic stress in gills of euryhaline milkfish. Since heat shock response is a predominant cellular stress response, two of its major components, heat shock protein 70 (HSP70) and 90 were examined in this study. Four hsp genes were first identified from the transcriptome database, divided into inducible (hsp under stress) and constitutive (hsp unstressed) forms. The alignment and phylogenetic analysis of the sequences revealed the four hsps (mfhsp) groups of milkfish, including mfhsp70, mfhsc70, mfhsp90α, and mfhsp90β. In addition, the mRNA and protein expression were examined through seawater (SW; 35‰) and freshwater (FW) acclimation experiments (> 1 month) and time-course (short term) experiments by direct transfer from SW to FW. In acclimation experiments, although the mRNA abundance of gill hsc70 of the FW-acclimated group was similar to that of the SW-acclimated group, gill hsp70 of the FW group was significantly higher (5.9 folds) than the SW group. Meanwhile, the mRNA abundacne of gill hsp90α of FW milkfish was slightly higher (1.5 folds) compared to the SW group, while the mRNA abundance of hsp90β was not different between the two groups. At the protein level, the abundance of HSP70 and HSP90 of milkfish gills were significantly higher (2.8 and 2.5 folds, respectively) in FW rather than in SW. On the other hand, analysis of gill hsp genes expression in short-term experiments revealed that gills hsc70 mRNA abundance increased within 3 hrs and declined gradually to 168 hrs. However, mRNA amounts of hsp70 and hsp90α rapidly increased at the first 3 hrs post-transfer (16 and 5.8 fold, respectively). Compared to the control group, the hsp90α showed significant increase at 168 hrs post-transfer, whereas hsp90β was not changed. The immunoblots revealed that relative abundance of gill HSP70 was significantly increased at 3 and 24 hrs post-transfer (about 4.3 and 3 folds, respectively). Relatvie protein amounts of the HSP90, however, were not significantly different even though the expression was still higher about 1.7 fold at 3 hrs post-transfer. The interaction between HSP70/90 and Na+, K+-ATPase (NKA), demonstrated by immunoprecipitation, indicated that increasing expression of gill HSPs might protect misfolded or abnormal NKA due to hypotonic stress of the milkfish. Taken together, our findings revealed that four hsps of milkfish displayed different patterns upon hypotonic stress. Higher expression of HSPs demonstrated that inducible HSP70/90 were more efficient in responses to hypotonic stress. The interaction between HSP70/90 and NKA further illustrated the involvement of HSPs in osmoprotective roles for maintaining cellular homeostasis of milkfish gills under hypotonic stress.
Book chapters on the topic "Hypotonic shock"
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Galietta, L. J. V., V. Barone, D. C. Gruenert, and G. Romeo. "A Chloride Conductance Evoked by Hypotonic Shock in Epithelial Cells." In Advances in Experimental Medicine and Biology, 307–17. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-5934-0_29.
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Mastrocola, Teresa, and Michela Rugolo. "The Response of Chloride Transport to Cyclic AMP, Calcium and Hypotonic Shock in Normal and Cystic Fibrosis Fibroblasts." In Advances in Experimental Medicine and Biology, 377–78. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-5934-0_43.
Full textConference papers on the topic "Hypotonic shock"
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Dagenais, Andre, Marie-Claude Tessier, Sabina Tatur, Ryszard Grygorczyk, and Yves Berthiaume. "Hypotonic Shock Increases Na+ Current Via A Cl-And Ca++ Dependent Mechanism In Alveolar Epithelial Cells." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a3531.
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Holme, S., W. A. Heaton, and P. Hartman. "INDIUM-111 PLATELET SURVIVAL STUDIES ON PLATELET CONCENTRATES (PCVSTORED FOR UP TO 14 DAYS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644690.
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The effect of extended storage on platelet in vitro and in vivo viability was investigated to determine the reliability and efficacy of Indium-111-oxine radiolabeling of long-term stored platelets. The fitness of various mathematical models for measurement of platelet survival and recovery was also evaluated.33 CPDA-1 PC were prepared and stored for various periods of time (see below) according to standard blood bank methods. The volume of the PC was adjusted to 65-75 mL to prevent pH fall with extended storage. After storage, samples were taken for in vitro assays and for radiolabeling witn Indium-111-oxine using standardized methods. None of the PC had pH<6.3. Afxer reinfusion of the labeled platelets, samples for measurement of radioactivity were taken at three hours and daily for seven days.The uptake {%) of Indium-111 and loss of platelets during the labeling showed no correlation with storage time; the means of the 33 studies were 71±8% and 35±6%, respectively. There was no significant correlation between the parameters and recovery or survival which suggests reliable labeling of nonviable platelets. Excellent fit of the survival data to the multiple hit gamma model was found forpall studies as determined by the coefficient of determination, r 2. The survival curves of platelets stored for one and five days were quite linear as shown by r2 ; with longer storage periods they became more exponential as shown by an increasingly better fit (r2 ) to the log model.Using the gamma model, both in vivo recovery and survival showed a progressive loss with increasing storage duration. This was less evident with the linear model. The loss of in vivo viability paralleled closely a decrease in the in vitro , parameters of platelet quality (discoid shape, hypotonic shock response, ATP content, and oxygen consumption) during storage.In conclusion, this study indicates that extended storage not only yields platelets with reduced recovery, but also platelets with shortened survival.