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1.
《Journal of Molluscan Studies》1965,36(6):323
WARBURG, M. R., 1965. On the water economy of some Australianland snails. Proc. malac. Soc. Lond. 36, 297305. Page 298: second line from bottom, should read within± 1 µg for Themapupa. Page 300: Fig. 2 legend, should read Evaporative waterloss from Sinumelon remissum (a), Pleuroxia sp. (b) and Themapupaadelaidae (c). Page 300: section 4 heading, should read Continuous curvesfor water loss. Page 301: second line, for Fig. 9 read Fig.3. Page 301: Table 1, last line, for 0.120024 read0.12024. Present address: Israel Institute for Biological Research, Ness-Ziona,Israel. 相似文献
2.
Sweeney WE Kusner L Carlin CR Chang S Futey L Cotton CU Dell KM Avner ED 《American journal of physiology. Cell physiology》2001,281(5):C1695-C1705
To study the pathophysiology ofautosomal recessive polycystic kidney disease (ARPKD), we soughtto develop conditionally immortalized control and cystic murinecollecting tubule (CT) cell lines. CT cells were isolated fromintercross breedings between BPK mice(bpk+/), a murine model of ARPKD,and the Immorto mice(H-2Kb-ts-A58+/+).Second-generation outbred offspring (BPK × Immorto) homozygous for the BPK mutation (bpk/;Im+/±; cysticBPK/H-2Kb-ts-A58), were phenotypicallyindistinguishable from inbred cystic BPK animals(bpk/). CysticBPK/H-2Kb-ts-A58 mice developed biliary ductalectasia and massively enlarged kidneys, leading to renal failure anddeath by postnatal day 24. Principal cells (PC) wereisolated from outbred cystic and noncystic BPK/H-2Kb-ts-A58 littermates at specificdevelopmental stages. Epithelial monolayers were under nonpermissiveconditions for markers of epithelial cell polarity and PC function.Cystic and noncystic cells displayed several properties characteristicof PCs in vivo, including amiloride-sensitive sodium transport andaquaporin 2 expression. Cystic cells exhibited apical epidermal growthfactor receptor (EGFR) mislocalization but normal expression of ZO-1 and E-cadherin. Hence, these cell lines retain the requisitecharacteristics of PCs, and cysticBPK/H-2Kb-ts-A58 PCs retained the abnormal EGFRmembrane expression characteristic of ARPKD. These cell lines representimportant new reagents for studying the pathogenesis of ARPKD. 相似文献
3.
《Journal of experimental botany》1980,31(6):1477
Volume 31, Number 123: The Effects of Leaf Age and Senescenceon the Distribution of Carbon in Lolium temulentum by E. J.Lloyd. Page 1074, Fig. 4 The final sentence of the legend should read:Ethanol extract: soluble, insoluble, in light (...)or in darkness (). Page 1079, line 6 In the reference to SMILLIE (1969), lth shouldread 1 lth. 相似文献
4.
Cell-attached recordings revealedK+ channel activity in basolateral membranes ofguinea pig distal colonic crypts. Inwardly rectified currents wereapparent with a pipette solution containing 140 mM K+.Single-channel conductance () was 9 pS at the resting membrane potential. Another inward rectifier with of 19 pS was observed occasionally. At a holding potential of 80 mV, was 21 and 41 pS,respectively. Identity as K+ channels was confirmed afterpatch excision by changing the bath ion composition. From reversalpotentials, relative permeability of Na+ overK+ (PNa/PK)was 0.02 ± 0.02, withPRb/PK = 1.1 andPCl/PK < 0.03. Spontaneous open probability (Po) of the 9-pSinward rectifier (gpKir) was voltageindependent in cell-attached patches. Both a low(Po = 0.09 ± 0.01) and a moderate(Po = 0.41 ± 0.01) activity mode wereobserved. Excision moved gpKir to the mediumactivity mode; Po ofgpKir was independent of bath Ca2+activity and bath acidification. Addition of Cl andK+ secretagogues altered Po ofgpKir. Forskolin or carbachol (10 µM)activated the small-conductance gpKir inquiescent patches and increased Po inlow-activity patches. K+ secretagogues, either epinephrine(5 µM) or prostaglandin E2 (100 nM), decreasedPo of gpKir in activepatches. This gpKir may be involved inelectrogenic secretion of Cl and K+ acrossthe colonic epithelium, which requires a large basolateral membraneK+ conductance during maximal Cl secretionand, presumably, a lower K+ conductance during primaryelectrogenic K+ secretion. 相似文献
5.
Cell cycle-related changes in transient K(+) current density in the GH3 pituitary cell line 总被引:2,自引:0,他引:2
Czarnecki A Vaur S Dufy-Barbe L Dufy B Bresson-Bepoldin L 《American journal of physiology. Cell physiology》2000,279(6):C1819-C1828
Our aim was to determinewhether the expression of K+ currents is related to thecell cycle in the excitable GH3 pituitary cell line. K+currents were studied by electrophysiology, and bromodeoxyuridine (BrdU) labeling was used to compare their expression in cells thereafter identified as being in the S or non-S phase of the cellcycle. We show that the peak density of the transient outward K+ current (Ito) was 33% lower incells in S phase (BrdU+) than in cells in other phases of the cellcycle (BrdU). The voltage-dependence of Itowas not modified. However, of the two kinetic components ofIto inactivation, the characteristics of thefast component differed significantly between BrdU+ and BrdU cells.Recovery from inactivation of Ito showedbiexponential and monoexponential function in BrdU and BrdU+ cells,respectively. This suggests that the molecular basis of this currentvaries during the cell cycle. We further demonstrated that4-aminopyridine, which blocks Ito, inhibited GH3cell proliferation without altering the membrane potential. These datasuggest that Ito may play a role in GH3 cellproliferation processes. 相似文献
6.
《Journal of experimental botany》1980,31(1):1
The publishers apologize for the following errors, which appearedin Plant Geosensors by L. J. Audus (pp. 10511073): Page 1058, line 9: the expression should read P = (L2/D)/(l/q) Page 1068, paragraph (c) line 11: should read reticulum, which was fairly uniformly peripheralin vertical roots, aggregated on the 相似文献
7.
Smith, J. R., Smith, F. A. and Walker, N. A. 1987. Potassiumtransport across the membrane of Chara. I. The relationshipbetween radioactive tracer influx and electrical conductance.J.exp. Bot. 38:731751. The 42K influx () and the electrical conductance (Gm) were measured simultaneously for the membraneof internodal cells of Chara australis as a function of theexternal [KCl] (K?. In bathing solutions of pH = 5?0, progressively increased from 20?5to 430?60 nmol m2 s1 and Gm increased from 0?36?0?02to 3?8?0?8 S m2 when K? was increased from 0?1 to 10mol m3. The resting membrane potential difference (p.d.)was approximately -135 mV for low K? and approached the expectedNernst equilibrium p.d. for K+ ions when K? > 1?0 mol m3.Measurements of 36Cl influx suggested that the 42K influx waspredominantly electrogenic. The equivalent Goldman permeabilityto K+ ions (Pk) was approximately 2030 nm s1 anddid not vary significantly with increasing K?. The equivalentconductance attributable to the electrogenic transport of K+ ions was calculated from assuming passive, independent diffusionof K+ ions and the ratio was found to be typically close to one. It was also found that themagnitudes of and Gm measuredsimultaneously for each individual cell were also well correlatedfor K? 1?0 mol m3, and that the slope of the line ofbest fit was close to one. For each K? it was found that theconductance not attributable to K+ translocation and presumablyassociated primarily with the transport of protons or theirequivalents was typically 0?20?5 Sm2. For K? >1?0 mol m3 the results indicated that the transport ofK+ ions was essentially independent, i.e. there was no evidencefor flux interactions. The results also indicated that the equivalentconductance derived from the measured 42K influx could usefullyindicate the fraction of the electrical conductance attributableto the translocation of K+ ions. Key words: Potassium, conductance, influx 相似文献
8.
Klaesner Joseph W.; Pou N. Adrienne; Parker Richard E.; Finney Charlene; Roselli Robert J. 《Journal of applied physiology》1997,83(6):1976-1985
Klaesner, Joseph W., N. Adrienne Pou, Richard E. Parker,Charlene Finney, and Robert J. Roselli. Optical measurement ofisolated canine lung filtration coefficients at normal hematocrits. J. Appl. Physiol. 83(6):1976-1985, 1997.In this study, lung filtration coefficient(Kfc) valueswere measured in eight isolated canine lung preparations at normalhematocrit values using three methods: gravimetric, blood-correctedgravimetric, and optical. The lungs were kept in zone 3 conditions andsubjected to an average venous pressure increase of 10.24 ± 0.27 (SE) cmH2O. The resulting Kfc(ml · min1 · cmH2O1 · 100 g dry lung wt1) measuredwith the gravimetric technique was 0.420 ± 0.017, which wasstatistically different from theKfc measured bythe blood-corrected gravimetric method (0.273 ± 0.018) or theproduct of the reflection coefficient(f) andKfc measuredoptically (0.272 ± 0.018). The optical method involved the use of aCellco filter cartridge to separate red blood cells from plasma, whichallowed measurement of the concentration of the tracer in plasma atnormal hematocrits (34 ± 1.5). The permeability-surface areaproduct was measured using radioactive multiple indicator-dilutionmethods before, during, and after venous pressure elevations. Resultsshowed that the surface area of the lung did not change significantlyduring the measurement ofKfc. Thesestudies suggest thatfKfccan be measured optically at normal hematocrits, that this measurement is not influenced by blood volume changes that occur during the measurement, and that the opticalfKfcagrees with theKfc obtained viathe blood-corrected gravimetric method. 相似文献
9.
Pharmacological activation of cloned intermediate- and small-conductance Ca(2+)-activated K(+) channels 总被引:1,自引:0,他引:1
Syme CA Gerlach AC Singh AK Devor DC 《American journal of physiology. Cell physiology》2000,278(3):C570-C581
We previouslycharacterized 1-ethyl-2-benzimidazolinone (1-EBIO), as well as theclinically useful benzoxazoles, chlorzoxazone (CZ), and zoxazolamine(ZOX), as pharmacological activators of the intermediate-conductanceCa2+-activated K+ channel, hIK1. The mechanismof activation of hIK1, as well as the highly homologoussmall-conductance, Ca2+-dependent K+ channel,rSK2, was determined following heterologous expression inXenopus oocytes using two-electrode voltage clamp (TEVC) and excised, inside-out patch-clamp techniques. 1-EBIO, CZ, and ZOX activated both hIK1 and rSK2 in TEVC and excised inside-out patch-clamp experiments. In excised, inside-out patches, 1-EBIO and CZ induced aconcentration-dependent activation of hIK1, with half-maximal (K1/2) values of 84 µM and 98 µM, respectively.Similarly, CZ activated rSK2 with a K1/2 of 87 µM. In the absence of CZ, the Ca2+-dependent activationof hIK1 was best fit with a K1/2 of 700 nM and aHill coefficient (n) of 2.0. rSK2 was activated byCa2+ with a K1/2 of 700 nM and ann of 2.5. Addition of CZ had no effect on either theK1/2 or n for Ca2+-dependentactivation of either hIK1 or rSK2. Rather, CZ increased channelactivity at all Ca2+ concentrations(Vmax). Event-duration analysis revealed hIK1 wasminimally described by two open and three closed times. Activation by1-EBIO had no effect on o1, o2, orc1, whereas c2 and c3 werereduced from 9.0 and 92.6 ms to 5.0 and 44.1 ms, respectively. Inconclusion, we define 1-EBIO, CZ, and ZOX as the first known activatorsof hIK1 and rSK2. Openers of IK and SK channels may be therapeuticallybeneficial in cystic fibrosis and vascular diseases. 相似文献
10.
Constable, Peter D. A simplified strong ion model foracid-base equilibria: application to horse plasma. J. Appl. Physiol. 83(1): 297-311, 1997.TheHenderson-Hasselbalch equation and Stewart's strong ion model arecurrently used to describe mammalian acid-base equilibria. Anomaliesexist when the Henderson-Hasselbalch equation is applied to plasma,whereas the strong ion model does not provide a practical method fordetermining the total plasma concentration of nonvolatile weak acids([Atot]) and theeffective dissociation constant for plasma weak acids(Ka). Asimplified strong ion model, which was developed from the assumptionthat plasma ions act as strong ions, volatile buffer ions(HCO3), or nonvolatile buffer ions,indicates that plasma pH is determined by five independent variables:PCO2, strong ion difference, concentration of individual nonvolatile plasma buffers (albumin, globulin, and phosphate), ionic strength, and temperature. The simplified strong ion model conveys on a fundamental level the mechanism for change in acid-base status, explains many of the anomalies when the Henderson-Hasselbalch equation is applied to plasma,is conceptually and algebraically simpler than Stewart's strong ionmodel, and provides a practical in vitro method for determining[Atot] andKa of plasma.Application of the simplified strong ion model toCO2-tonometered horse plasmaproduced values for[Atot] (15.0 ± 3.1 meq/l) and Ka(2.22 ± 0.32 × 107 eq/l) that weresignificantly different from the values commonly assumed for humanplasma ([Atot] = 20.0 meq/l, Ka = 3.0 × 107 eq/l).Moreover, application of the experimentally determined values for[Atot] andKa to publisheddata for the horse (known PCO2,strong ion difference, and plasma protein concentration) predictedplasma pH more accurately than the values for[Atot] andKa commonlyassumed for human plasma. Species-specific values for[Atot] andKa should beexperimentally determined when the simplified strong ion model (orstrong ion model) is used to describe acid-base equilibria. 相似文献
11.
A distributed nonlinear model of lung tissue elasticity 总被引:2,自引:0,他引:2
Maksym, Geoffrey N., and Jason H. T. Bates. Adistributed nonlinear model of lung tissue elasticity.J. Appl. Physiol. 82(1): 32-41, 1997.- We present a theory relating the static stress-strainproperties of lung tissue strips to the stress-bearing constituents,collagen and elastin. The fiber pair is modeled as a Hookean spring(elastin) in parallel with a nonlinear string element (collagen), whichextends to a maximum stop length. Based on a series of fiber pairs, wedevelop both analytical and numerical models with distributedconstituent properties that account for nonlinear tissue elasticity.The models were fit to measured stretched stress-strain curves of fiveuniaxially stretched tissue strips, each from a different dog lung. Wefound that the distributions of stop length and spring stiffness followinverse power laws, and we hypothesize that this results from thecomplex fractal-like structure of the constituent fiber matrices inlung tissue. We applied the models to representative pressure-volume(PV) curves from patients with normal, emphysematous,and fibrotic lungs. The PV curves were fit to theequation V = A Bexp(KP),where V is volume, P is transpulmonary pressure, andA, B, andK are constants. Our models lead to apossible mechanistic explanation of the shape factorK in terms of the structuralorganization of collagen and elastin fibers. 相似文献
12.
Devor Daniel C.; Frizzell Raymond A. 《American journal of physiology. Cell physiology》1998,274(1):C149
We usedsingle-channel recording techniques to identify and characterize alarge-conductance,Ca2+-independentK+ channel in the colonicsecretory cell line T84. In symmetric potassium gluconate, this channelhad a linear current-voltage relationship with a single-channelconductance of 161 pS. Channel open probability(Po) wasincreased at depolarizing potentials. Partial substitution of bathK+ withNa+ indicated a permeability ratioof K+ toNa+ of 25:1. ChannelPo was reduced byextracellular Ba2+. Event-durationanalysis suggested a linear kinetic model for channel gating having asingle open state and three closed states: C3C2C1O.Arachidonic acid (AA) increased thePo of thechannel, with an apparent stimulatory constant(Ks)of 1.39 µM. Neither channel open time (O) nor the fast closed time(C1) was affected by AA. Incontrast, AA dramatically reduced mean closed time by decreasing bothC3 andC2. Thecis-unsaturated fatty acid linoleate increased Poalso, whereas the saturated fatty acid myristate and thetrans-unsaturated fatty acid elaidatedid not affectPo. This channelis activated also by negative pressure applied to the pipette duringinside-out recording. Thus we determined the effect of thestretch-activated channel blockers amiloride and Gd3+ on theK+ channel after activation by AA.Amiloride (2 mM) on the extracellular side reduced single-channelamplitude in a voltage-dependent manner, whereasGd3+ (100 µM) had no effect onchannel activity. Activation of this K+ channel may be important duringstimulation of Cl secretionby agonists that use AA as a second messenger (e.g., vasoactiveintestinal polypeptide, adenosine) or during the volume regulatoryresponse to cell swelling. 相似文献
13.
《Journal of Molluscan Studies》1895,1(7):337
Page 156, line 18, for "Antwerp" (Anvers) read "Auvers, 17 milesnorth-west of Paris." 相似文献
14.
Molecular and kinetic alterations of muscle AMP deaminase during chronic creatine depletion 总被引:2,自引:0,他引:2
Rush James W.E.; Tullson Peter C.; Terjung Ronald L. 《American journal of physiology. Cell physiology》1998,274(2):C465
We examined apossible mechanism to account for the maintenance of peak AMPdeamination rate in fast-twitch muscle of rats fed the creatine analog-guanidinopropionic acid (-GPA), in spite of reduced abundance ofthe enzyme AMP deaminase (AMPD). AMPD enzymatic capacity (determined atsaturating AMP concentration) and AMPD protein abundance (Western blot)were coordinately reduced ~80% in fast-twitch white gastrocnemiusmuscle by -GPA feeding over 7 wk. Kinetic analysis of AMPD in thesoluble cell fraction demonstrated a single Michaelis-Menten constant(Km; ~1.5 mM) in control muscle extracts. An additional high-affinityKm (~0.03 mM)was revealed at low AMP concentrations in extracts of -GPA-treated muscle. The kinetic alteration in AMPD reflects increased molecular activity at low AMP concentrations; this could account for high ratesof deamination in -GPA-treated muscle in situ, despite the loss ofAMPD enzyme protein. The elimination of this kinetic effect bytreatment of -GPA-treated muscle extracts with acid phosphatase invitro suggests that phosphorylation is involved in the kinetic controlof skeletal muscle AMPD in vivo. 相似文献
15.
Owing to a typographical error three equations were omittedfrom page 1294. The correct paragraphs are set out below. The component K1 corrected for the difference in temperaturebetween the enzyme assay and the leaf and was calculated accordingto the Arrhemus equation.
where v10 and v18 are the reaction velocities of carboxylationat 10?C and 18?C, respectively and A is the activation energy(A = 90 kJ mol1, as determined for purified wheat RuBPCOby M?chler, Keys and Cornelius, 1980) The components K2 corrected for the difference in CO2 partialpressure between enzyme assay and leaf and for competitive inhibitionof carboxylation by O2 and was calculated according to the modifiedMichaelis Menten equation
where vc, is the carboxylation velocity under leaf conditions,Vc. is the maximum carboxylation velocity as determined in theenzyme assay, Kc, and Ko are the Michaelis constants for carboxylationand oxygenation, respectively (Ko = 159 Pa CO2. Ko = 35.3 kPaO2, as interpolated for 18?C from spinach data as determinedby Jordan and Ogren, 1984), O is oxygen partial pressure inair and C1 is intercellular CO2 partial pressure in leaves (C1= 29.1 ? 0.8 Pa (? s c , n = 15)) The component K3 corrected for the decrease in CO2 fixationin leaves due to photorespiration and was calculated accordingto equation 3
Equation 3 is denved from the equation for the substrate specificityof RuBPCO, S= vc/voC (Laing, Ogren, and Hageman, 1974), andfrom the equation for the stoichiometry of photorespiratoryCO2 release, F=vc1/2 vo, where vc, and vc are reactionvelocities of carboxylation and oxygenation, O and C are partialpressures of 02 and intercellular CO2, F is net photosynthesisand S is the substrate specificity of RuBPCO (S= 3061 Pa/Pa,as interpolated for 18?C from spinach data as determined byJordan and Ogren, 1984) 相似文献
16.
Gadolinium prevents high airway pressure-induced permeability increases in isolated rat lungs 总被引:10,自引:0,他引:10
Parker James C.; Ivey Claire L.; Tucker J. Allan 《Journal of applied physiology》1998,84(4):1113-1118
To determine theinitial signaling event in the vascular permeability increase afterhigh airway pressure injury, we compared groups of lungs ventilated atdifferent peak inflation pressures (PIPs) with (gadolinium group) andwithout (control group) infusion of 20 µM gadolinium chloride, aninhibitor of endothelial stretch-activated cationchannels. Microvascular permeability was assessed by using the capillary filtration coefficient(Kfc), ameasure of capillary hydraulic conductivity.Kfc was measuredafter ventilation for 30-min periods with 7, 20, and 30 cmH2O PIP with 3 cmH2O positive end-expiratorypressure and with 35 cmH2O PIPwith 8 cmH2O positive end-expiratory pressure. In control lungs,Kfc increasedsignificantly to 1.8 and 3.7 times baseline after 30 and 35 cmH2O PIP, respectively. In thegadolinium group,Kfc was unchangedfrom baseline (0.060 ± 0.010 ml · min1 · cmH2O1 · 100 g1) after any PIPventilation period. Pulmonary vascular resistance increasedsignificantly from baseline in both groups before the lastKfc measurementbut was not different between groups. These results suggest thatmicrovascular permeability is actively modulated by a cellular responseto mechanical injury and that stretch-activated cation channels mayinitiate this response through increases in intracellular calciumconcentration. 相似文献
17.
Monocytic cell necrosis is mediated by potassium depletion and caspase-like proteases 总被引:2,自引:0,他引:2
Apoptosis is aphysiological cell death that culminates in mitochondrial permeabilitytransition and the activation of caspases, a family of cysteineproteases. Necrosis, in contrast, is a pathological cell deathcharacterized by swelling of the cytoplasm and mitochondria and rapidplasma membrane disruption. Necrotic cell death has long been opposedto apoptosis, but it now appears that both pathways involvemitochondrial permeability transition, raising the question of whatmediates necrotic cell death. In this study, we investigated mechanismsthat promote necrosis induced by various stimuli(Clostridium difficile toxins,Staphylococcus aureus alpha toxin,ouabain, nigericin) in THP-1 cells, a human monocytic cell line, and in monocytes. All stimuli induced typical features of necrosis and triggered protease-mediated release of interleukin-1 (IL-1) andCD14 in both cell types. K+depletion was actively implicated in necrosis because substituting K+ forNa+ in the extracellular mediumprevented morphological features of necrosis and IL-1 release.N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone, a broad-spectrum caspase inhibitor, prevented morphological features of necrosis, plasma membrane destruction, loss ofmitochondrial membrane potential, IL-1 release, and CD14 sheddinginduced by all stimuli. Thus, in monocytic cells, necrosis is a celldeath pathway mediated by passiveK+ efflux and activation ofcaspase-like proteases. 相似文献
18.
Functional characterization of the neuronal-specific K-Cl cotransporter: implications for [K+]o regulation 总被引:2,自引:0,他引:2
The neuronal K-Cl cotransporter isoform (KCC2) was functionallyexpressed in human embryonic kidney (HEK-293) cell lines. Two stablytransfected HEK-293 cell lines were prepared: one expressing anepitope-tagged KCC2 (KCC2-22T) and another expressing theunaltered KCC2 (KCC2-9). The KCC2-22T cells produced aglycoprotein of ~150 kDa that was absent from HEK-293 control cells.The 86Rb influx in both cell lineswas significantly greater than untransfected control HEK-293 cells. TheKCC2-9 cells displayed a constitutively active86Rb influx that could beincreased further by 1 mMN-ethylmaleimide (NEM) but not by cellswelling. Both furosemide [inhibition constant (Ki) ~25µM] and bumetanide (Ki~55 µM) inhibited the NEM-stimulated 86Rb influx in the KCC2-9cells. This diuretic-sensitive86Rb influx in theKCC2-9 cells, operationally defined as KCC2 mediated, required external Clbut not external Na+ and exhibiteda high apparent affinity for externalRb+(K+)[Michaelis constant(Km) = 5.2 ± 0.9 (SE) mM; n = 5] but alow apparent affinity for externalCl(Km >50 mM). Onthe basis of thermodynamic considerations as well as the unique kineticproperties of the KCC2 isoform, it is hypothesized that KCC2 may servea dual function in neurons: 1) themaintenance of low intracellularCl concentration so as toallow Cl influx vialigand-gated Cl channelsand 2) the buffering of externalK+ concentration([K+]o) in the brain. 相似文献
19.
Ca2+ influx inhibits voltage-dependent and augments Ca2+-dependent K+ currents in arterial myocytes 总被引:6,自引:0,他引:6
These experiments were performed to determine the effects ofreducing Ca2+ influx(Cain) onK+ currents(IK) inmyocytes from rat small mesenteric arteries by1) adding externalCd2+ or2) lowering externalCa2+ to 0.2 mM. When measured froma holding potential (HP) of 20 mV(IK20),decreasing Cain decreasedIK at voltageswhere it was active (>0 mV). When measured from a HP of 60 mV(IK60),decreasing Cain increasedIK at voltagesbetween 30 and +20 mV but decreased IK at voltagesabove +40 mV. Difference currents(IK) weredetermined by digital subtraction of currents recorded under controlconditions from those obtained whenCain was decreased. At testvoltages up to 0 mV,IK60 exhibitedkinetics similar to controlIK60, with rapidactivation to a peak followed by slow inactivation. At 0 mV, peakIK60 averaged75 ± 13 pA (n = 8) withCd2+ and 120 ± 20 pA(n = 9) with lowCa2+ concentration. At testvoltages from 0 to +60 mV,IK60 always had an early positive peak phase, but its apparent "inactivation" increased with voltage and its steady value became negative above +20mV. At +60 mV, the initial peakIK60 averaged115 ± 18 pA with Cd2+ and 187 ± 34 pA with low Ca2+. With 10 mM pipette BAPTA, Cd2+ produced asmall inhibition ofIK20 but stillincreased IK60 between 30 and +10 mV. InCa2+-free external solution,Cd2+ only decreased bothIK20 andIK60. In thepresence of iberiotoxin (100 nM) to inhibitCa2+-activatedK+ channels(KCa),Cd2+ increasedIK60 at allvoltages positive to 30 mV while BAY K 8644 (1 µM) decreasedIK60. Theseresults suggest that Cain, through L-type Ca2+ channels and perhapsother pathways, increases KCa(i.e., IK20) and decreases voltage-dependent K+currents in this tissue. This effect could contribute to membrane depolarization and force maintenance. 相似文献
20.
PGE1, dexamethasone, U-74389G, or Bt2-cAMP as an additive to promote protection by UW solution in I/R injury 总被引:1,自引:0,他引:1
Chiang Chi-Huei; Hsu Kang; Yan Horng-Chin; Harn Horng-Jyh; Chang Deh-Ming 《Journal of applied physiology》1997,83(2):583-590
Chiang, Chi-Huei, Kang Hsu, Horng-Chin Yan, Horng-Jyh Harn,and Deh-Ming Chang.PGE1, dexamethasone,U-74389G, or Bt2-cAMP as anadditive to promote protection by UW solution in I/R injury. J. Appl. Physiol. 83(2): 583-590, 1997.A method to reduce ischemia-reperfusion (I/R) injury can be animportant criterion to improve the preservation solution. AlthoughUniversity of Wisconsin solution (UW) works as a lung preservationsolution, its attenuation effect on I/R injury has not beeninvestigated. We attempted to determine whether, by adding variousprotective agents, modified UW solutions will enhance the I/Rattenuation by UW. We examined the I/R injury in an isolated rat lungmodel. Various solutions, e.g., physiological salt solution (PSS), UW,and modified UW solutions containing various protective agents such asprostaglandin E1, dexamethasone, U-74389G, or dibutyryl adenosine 3,5-cyclic monophosphatewere perfused individually to evaluate the I/R injury. Isolated rat lung experiments, with ischemia for 45 min, then reperfusion for 60 min, were conducted in a closed circulating system.Hemodynamic changes, lung weight gain (LWG), capillary filtrationcoefficient (Kfc), proteincontent of lavage fluid, concentration of cytokines, and lunghistopathology were analyzed. Results showed that the acute I/R lunginjury with immediate permeability pulmonary edema was associated withan increase in tumor necrosis factor- (TNF-) production. A significant correlation existed betweenTNF- and Kfc(r = 0.8, P < 0.0001) and TNF- and LWG(r = 0.9, P < 0.0001), indicatingthat TNF- is an important cytokine modulating early I/R injury.Significantly lower levels ofKfc, LWG,TNF-, and protein concentration of lung lavage(P < 0.05) were found in theUW-perfused group than in the control group perfused with PSS. ModifiedUW promoted the protective effect of UW to further decreaseKfc, LWG, andTNF- (P < 0.05).Histopathological observations also substantiated this evidence. In theUW+U-74389G group, bronchial alveolar lavage fluid contained lowestprotein concentration. We conclude that the UW solution attenuates I/Rinjury of rat lung and that the modified UW solutions further enhancethe effect of UW in reducing I/R injury. Among modified solutions,UW+U-74389G is the best. Further investigation of the improved effectsof the modified UW solutions would be beneficial in lungtransplantation. 相似文献