Concentration-response relationship of alpha 1-adrenoceptor-stimulated increase of 86Rb+ efflux in rat heart

The aim of the present study was to establish a concentration-response relationship for the alpha 1-adrenoceptor mediated increase of 86Rb+ efflux, and to characterize the sensitivity of this response to the selective alpha 1-adrenoceptor antagonist prazosin. Isolated rat hearts were perfused retrogradely at constant flow and at 31 degrees. Timolol (10(-6) mol/l) was used to block beta-adrenoceptors. After a loading period with 86Rb+ and 55 min. washout, the hearts were exposed to phenylephrine in a concentration range from 3 x 10(-8) mol/l to 10(-4) mol/l. Control experiments comparing the effects of alpha 1-adrenoceptor stimulation on 86Rb+ efflux and 42K+ efflux were performed. alpha 1-Adrenoceptor stimulation increased the 86Rb+ efflux with a pD2 = 6.35 +/- 0.20 (mean +/- S.E.M). The maximal response to phenylephrine was 22.5 +/- 2.0% (mean +/- S.E.M.) of the control values. The concentration-response curve was shifted to higher concentration of agonist in the presence of the alpha 1-adrenoceptor antagonist prazosin (3 x 10(10) mol/l). The calculated inhibition constant for prazosin was 6.1 x 10(-11) mol/l. 86Rb+ was found to be a suitable K+ analogue in the study of relative changes in K+ efflux although the basal efflux kinetics were different for the two isotopes. CONCLUSION: Phenylephrine increased the 86+b+ efflux concentration-dependently. A high sensitivity to prazosin confirmed the involvement of the alpha 1-adrenoceptor population.     

A transient outward-rectifying K+ channel current down-regulated by cytosolic Ca2+ in Arabidopsis thaliana guard cells

Sustained (noninactivating) outward-rectifying K+ channel currents have been identified in a variety of plant cell types and species. Here, in Arabidopsis thaliana guard cells, in addition to these sustained K+ currents, an inactivating outward-rectifying K+ current was characterized (plant A-type current: IAP). IAP activated rapidly with a time constant of 165 ms and inactivated slowly with a time constant of 7.2 sec at +40 mV. IAP was enhanced by increasing the duration (from 0 to 20 sec) and degree (from +20 to -100 mV) of prepulse hyperpolarization. Ionic substitution and relaxation (tail) current recordings showed that outward IAP was mainly carried by K+ ions. In contrast to the sustained outward-rectifying K+ currents, cytosolic alkaline pH was found to inhibit IAP and extracellular K+ was required for IAP activity. Furthermore, increasing cytosolic free Ca2+ in the physiological range strongly inhibited IAP activity with a half inhibitory concentration of approximately 94 nM. We present a detailed characterization of an inactivating K+ current in a higher plant cell. Regulation of IAP by diverse factors including membrane potential, cytosolic Ca2+ and pH, and extracellular K+ and Ca2+ implies that the inactivating IAP described here may have important functions during transient depolarizations found in guard cells, and in integrated signal transduction processes during stomatal movements.     

K+] dependence of open-channel conductance in cloned inward rectifier potassium channels (IRK1, Kir2.1)

Potassium conduction through unblocked inwardly rectifying (IRK1, Kir2.1) potassium channels was measured in inside-out-patches from Xenopus oocytes, after removal of polyamine-induced strong inward rectification. Unblocked IRK1 channel current-voltage (I-V) relations show very mild inward rectification in symmetrical solutions, are linearized in nonsymmetrical solutions that bring the K+ reversal potential to extreme negative values, and follow Goldman-Hodgkin-Katz constant field equation at extreme positive E alpha. When intracellular K+ concentration (KIN) was varied, at constant extracellular K+ concentration (KOUT) the conductance at the reversal potential (GREV) followed closely the predictions of the Goldman-Hodgkin-Katz constant field equation at low concentrations and saturated sharply at concentrations of > 150 mM. Similarly, when KOUT was varied, at constant KIN, GREV saturated at concentrations of > 150 mM. A square-root dependence of conductance on KOUT is a well-known property of inward rectifier potassium channels and is a property of the open channel. A nonsymmetrical two-site three-barrier model can qualitatively explain both the I-V relations and the [K+] dependence of conductance of open IRK1 (Kir2.1) channels.     

烧结矿粒度组成对竖冷炉运行影响的DEM模拟

 为改善竖冷炉内空隙率分布,促进矿气接触换热,从降低烧结矿入炉粒度上限的角度设计了粒度分布范围逐渐减小的3种工况,并以梅钢竖冷炉单个炉腔准三维扁平模型为基础,采用离散单元法模拟研究了炉内烧结矿流速分布、空隙率分布和压降分布的变化规律。结果表明,采用10～150 mm的入炉粒度组成,中心风帽上方会形成矩形低速区,降低烧结矿下移速度的均匀性;低空隙率区逐渐扩大,并形成炉腔中间区空隙率较低,边缘和中心区空隙率较高的分布。炉内空隙率偏析最严重,分布均匀性最差;炉内40%区域为高压降区,主要分布在炉腔中间区;20%区域为低压降区,主要分布在炉腔中心区,造成炉内气流偏析亦最严重。减少入炉粒度上限后,矩形低速区得以消除,烧结矿流动整体性得以提高;当采用10～90 mm的入炉粒度组成时,可以提高空隙率最小值,并降低炉腔中间区与边壁和中心区空隙率的差值,使得空隙率的偏析程度最小,均匀性最高;同时能够降低压降的最大值、提高最小值,并扩大中压降区范围,从而缓解炉内气流偏析分布,提高其分布的均匀性。通过增设二次破碎工艺降低烧结矿入炉粒度上限可以成为改善烧结矿竖冷炉运行的一种实践方向,今后应开展最适宜的烧结矿入炉粒度范围及各粒度段质量分数的研究。     

The left ventricular contractility of the rat heart is modulated by changes in flow and alpha 1-adrenoceptor stimulation

Myocardial contractility depends on several mechanisms such as coronary perfusion pressure (CPP) and flow as well as on alpha 1-adrenoceptor stimulation. Both effects occur during the sympathetic stimulation mediated by norepinephrine. Norepinephrine increases force development in the heart and produces vasoconstriction increasing arterial pressure and, in turn, CPP. The contribution of each of these factors to the increase in myocardial performance needs to be clarified. Thus, in the present study we used two protocols: in the first we measured mean arterial pressure, left ventricular pressure and rate of rise of left ventricular pressure development in anesthetized rats (N = 10) submitted to phenylephrine (PE) stimulation before and after propranolol plus atropine treatment. These observations showed that in vivo alpha 1-adrenergic stimulation increases left ventricular developed pressure (P < 0.05) together with arterial blood pressure (P < 0.05). In the second protocol, we measured left ventricular isovolumic systolic pressure (ISP) and CPP in Langendorff constant flow-perfused hearts. The hearts (N = 7) were perfused with increasing flow rates under control conditions and PE or PE + nitroprusside (NP). Both CPP and ISP increased (P < 0.01) as a function of flow. CPP changes were not affected by drug treatment but ISP increased (P < 0.01). The largest ISP increase was obtained with PE + NP treatment (P < 0.01). The results suggest that both mechanisms, i.e., direct stimulation of myocardial alpha 1-adrenoceptors and increased flow, increased cardiac performance acting simultaneously and synergistically.     

Cesium effects on i(f) and i(K) in rabbit sinoatrial node myocytes: implications for SA node automaticity

Cesium blocks the hyperpolarization-activated current i(f) but blocks neither the delayed-rectifier current i(K) nor the sinoatrial (SA) node discharge. It has been proposed that the failure of Cs+ to block SA discharge is either an incomplete block or a negative shift of i(f). However, an alternative possibility is that i(K) (rather than i(f)) has a predominant role in the SA-pacemaker potential. To investigate this point, the effects of Cs+ on both i(f) and i(K) in the pacemaker range of potentials were studied in the same single SA node cell at the same time by means of the perforated patch-clamp technique. Hyperpolarizing steps from a holding potential (Vh) of -35 mV into and past the pacemaker-potential range resulted in a progressively larger i(f) associated with an increasing slope conductance. Cs+ (2 mM) reversibly blocked both i(f) and the slope conductance increase, suggesting that the current activated was indeed predominantly i(f). Subsequently, hyperpolarizing steps to -50, -60, and -70 mV were applied in the absence (to activate only i(f)) and in the presence of a prior depolarizing step to +10 mV (to activate i(K) as well, as the action potential normally does). Cs+ almost abolished i(f) but only slightly decreased i(K). It is concluded that the failure of Cs+ to block the SA- node spontaneous discharge is not due to a shift of i(f) out of the pacemaker range (due to run-down) or an incomplete block of i(f). Instead, the resistance of i(K) to block by Cs+ is consistent with a predominant role of i(K) for the discharge of the SA node, although i(f) can contribute under normal or special circumstances. The reduction of i(K) by Cs+ raises the question whether the Cs+ slows the SA-node discharge not only by suppressing I(f), but also by reducing i(K).     

Activation of alpha 2-adrenoceptors causes inhibition of calcium channels but does not modulate inwardly-rectifying K+ channels in caudal raphe neurons

Many neurotransmitter receptors that interact with pertussis toxin-sensitive G proteins, including the alpha 2-adrenergic receptor, can modulate both voltage-dependent calcium channels and G protein-coupled inwardly-rectifying K+ channels. Serotonergic neurons of the medulla oblongata (nucleus raphe obscurus and nucleus raphe pallidus), which provide a major projection to sympathetic and motor output systems, receive a catecholaminergic input and express alpha 2-adrenergic receptors. Therefore, we tested the effects of norepinephrine on voltage-dependent calcium channels and G protein-coupled inwardly-rectifying K+ channels in neonatal raphe neurons using whole-cell recording in a brainstem slice preparation. Calcium channel currents were inhibited by norepinephrine in the majority of raphe neurons tested (88%) and in all identified tryptophan hydroxylase-immunoreactive (i.e. serotonergic) neurons. When tested in the same neurons, the magnitude of calcium current inhibition by norepinephrine (approximately 25%) was less than that induced by 5-hydroxytryptamine (approximately 50%). The norepinephrine-induced calcium current inhibition was mediated by alpha 2-adrenergic receptors; it was mimicked by UK 14304, an alpha 2-adrenergic receptor agonist and blocked by idazoxan, an alpha 2-adrenergic receptor antagonist, but not affected by prazosin or propanolol (alpha 1 and beta adrenergic antagonists, respectively). Calcium current inhibition by norepinephrine was essentially eliminated following application of omega-Conotoxin GVIA and omega-Agatoxin IVA, indicating that norepinephrine modulated N- and P/Q-type calcium channels predominantly. Calcium current inhibition by norepinephrine was voltage-dependent and mediated by pertussis toxin-sensitive G proteins. Thus, as expected, alpha 2-adrenergic receptor activation inhibited N- and P/Q-type calcium currents in medullary raphe neurons via pertussis toxin-sensitive G proteins. In parallel experiments, however, we found that norepinephrine had no effect on G protein-coupled inwardly-rectifying K+ channels in any raphe neurons tested, despite the robust activation of those channels in the same neurons by 5-hydroxytryptamine. Together, these data indicate that alpha 2-adrenergic receptors can modulate N- and P/Q-type calcium channels in caudal medullary raphe neurons but do not couple to the G protein-coupled inwardly-rectifying K+ channels which are also present in those cells. This is in contrast to the effect of 5-hydroxytryptamine1A receptor activation in caudal raphe neurons, and indicates a degree of specificity in the signalling by different pertussis toxin-sensitive G protein-coupled receptors to voltage-dependent calcium channels and G protein-coupled inwardly-rectifying K+ channels even within the same cell system.     

The kinetics of extracellular potassium changes during hypoxia and anoxia in the cat cerebral cortex

Extracellular potassium activity, [K+]0, was continuously measured using potassium specific microelectrodes in the cerebral cortex of cats before and after hypoxic or anoxic insults. Two patterns of [K+]0 increase were seen. A slow, linear rise occurred during hypoxia and hypothermia and was correlated with changes in mean blood pressure (B/P). A fast, complex, exponential rise resembling spreading depression occurred during anoxia and was unassociated with B/P changes. The fall of [K+]0 after reversal of the insult was described by a single exponential function with rate constants from 0.009 to 0.0194 sec-1. It is suggested that the linear rise is primarily a result of sodium pump inhibition and that the exponential rise is due to a superimposed sudden increase in cell membrane permeability perhaps secondary to transmitter release. The kinetics of the fall of [K+[0 is consistent with the normalization of the sodium and potassium gradients across the cell membranes secondary to Na+-K+ATPase activity.     

Expression environment determines K+ current properties: Kv1 and Kv4 alpha-subunit-induced K+ currents in mammalian cell lines and cardiac myocytes

Voltage-gated K+ channel (Kv) pore-forming (alpha) subunits of the Kv1 and Kv4 subfamilies have been cloned from heart cDNA libraries, and are thought to play roles in the generation of the transient outward K+ current, Ito. Heterologous expression of these subunits in Xenopus oocytes, however, reveals K+ currents that are quite distinct from Ito. In the experiments here, the detailed time- and voltage-dependent properties of the currents expressed in mammalian cell lines and in cardiac myocytes by Kv1.4 and Kv4.2 were examined and compared to previous findings in studies of oocytes, as well as to Ito characterized in various myocardial cells. As in oocytes, expression of Kv1.4 in HEK-293, Ltk- or neonatal rat ventricular cells reveals rapidly activating K+ currents. In contrast to the currents in oocytes, however, there are two components of inactivation of the Kv1.4-induced currents in mammalian cells, and both components are significantly slower in myocytes than in either HEK-293 or Ltk- cells. In addition, in all three cell types, recovery of Kv1.4 from steady-state inactivation is very slow, proceeding with mean time constants in the range of 6-8 s. The properties of Kv4.2-induced currents also vary with cell type and, importantly, the rates of activation, inactivation and recovery from inactivation are significantly faster in mammalian cells than in Xenopus oocytes. In HEK-293, Chinese hamster ovary (CHO) and neonatal rat ventricular cells, for example, the currents recover from steady-state inactivation with mean (+/-SD) time constants of 153+/-32 (n=12), 245+/-112 (n=10) and 86+/-38 (n=11) ms, respectively; therefore, recovery proceeds 5-10 times faster than observed for Kv4.2 in oocytes. These results emphasize the importance of the cellular expression environment in efforts to correlate endogenous K+ currents with heterologously expressed K+ channel subunits. In addition, the finding that Kv alpha subunits produce distinct K+ currents in different cells suggests that cell-type-specific associations with endogenous Kv alpha or accessory beta subunits and/or post-translational processing play roles in determining the properties of functional K+ channels.     

Effects of Moisture on Pyrolysis of Polypropylene

The thermal degradation kinetics of polypropylene (PP) in steam was investigated with a thermal gravimetric analysis (TGA) reaction system. The experiments were carried out in the 500–800 K temperature range at various constant heating rates of 1, 2, and 5 K∕min. The partial pressure of steam in the system was adjusted to 0.24 atm, which is seen in most municipal solid waste (MSW) incinerators in Taiwan. The results indicated that the water molecule significantly enhanced the thermal degradation rate of PP. The corresponding activation energy, preexponential factor, and reaction order were determined. It was found that thermal degradation of PP in steam can be adequately described by an overall rate equation.     

Kinetics of leaching of lead sulfate in sodium chloride solutions

A powder dissolution method is used to study the kinetics of leaching of lead sulfate from a lead cake in the temperature range 298–353 K and the concentration range 50–270 g/l of a sodium chloride solution. The results obtained are used to calculate the apparent activation energy (E _a = 12.41 kJ/mol); its value indicates that the process of leaching of lead sulfate from a lead cake occurs in a diffusion zone. This process is shown to be described by a first-order kinetic equation.     

In vivo functional role of the Drosophila hyperkinetic beta subunit in gating and inactivation of Shaker K+ channels

The physiological roles of the beta, or auxiliary, subunits of voltage-gated ion channels, including Na+, Ca2+, and K+ channels, have not been demonstrated directly in vivo. Drosophila Hyperkinetic (Hk) mutations alter a gene encoding a homolog of the mammalian K+ channel beta subunit, providing a unique opportunity to delineate the in vivo function of auxiliary subunits in K+ channels. We found that the Hk beta subunit modulates a wide range of the Shaker (Sh) K+ current properties, including its amplitude, activation and inactivation, temperature dependence, and drug sensitivity. Characterizations of the existing mutants in identified muscle cells enabled an analysis of potential mechanisms of subunit interactions and their functional consequences. The results are consistent with the idea that via hydrophobic interaction, Hk beta subunits modulate Sh channel conformation in the cytoplasmic pore region. The modulatory effects of the Hk beta subunit appeared to be specific to the Sh alpha subunit because other voltage- and Ca(2+)-activated K+ currents were not affected by Hk mutations. The mutant effects were especially pronounced near the voltage threshold of IA activation, which can disrupt the maintenance of the quiescent state and lead to the striking neuromuscular and behavioral hyperexcitability previously reported.     

Activities of oxygen in liquid copper and silver from electrochemical measurements

Modified coulometric titrations on the galvanic cell:O in liquid Cu or Ag / ZrO₂( + CaO) / Air, Pt, were performed to determine precisely the oxygen activities in liquid copper and silver in the range of relatively low oxygen concentration. The present experimental results were remarkably reproducible in comparison with the published data. The standard Gibbs energies of solution of oxygen in liquid copper and liquid silver for 1/2 O₂(l atm) → O(l at. pct) were determined respectively to be ΔG° (in Cu) = −18040 −0.03 T(K) (± 120) cal · g-atom−1 = −75500 −0.12 T(K)(± 500) J · g-atom−1, ΔG°(inAg)= -3860+ 1.56 T(K) (±90) cal · g-atom−1 = −16140 + 6.52 T(K)(±380) J · g-atom−1 where the reference state for dissolved oxygen was an infinitely dilute solution. The present value of the partial entropy of oxygen dissolved in liquid copper differs significantly from that suggested by many investigators. Further, the present equation for liquid copper has been found to be consistent with a correlation proposed previously by the present authors. The equation for liquid silver is in good agreement with the published ones.     

The effect of pressure on the electrical breakdown in the membranes of Valonia utricularis

The interpretation of electrical breakdown in terms of electro-mechanical instabilities, predicts that the breakdown potential should decrease with increasing cell turgor pressure. Experiments were conducted to test this hypothesis on cells of Valonia utricularis over a turgor pressure range of 0.5-10(5)-5.0-10(5) N/m2. Electrical breakdown was measured using intracellular electrodes and 500 mus current pulses. The pressure was monitored by an intracellular micropipette pressure transducer. The results obtained show a linear decrease in the critical breakdown potential with pressure. The effective compressive modulus of the cell membrane, gamma, is calculated from the slope of this line to 69+/-10-10(5) N/m2 (average value of seven measurements). This is consistent with the theoretical prediction of the electromechanical model using our previously determined values of the elastic modulus of the membrane. A theoretical analysis is given of the effects of pressure on the breakdown, This includes also considerations of the indirect effect of pressure on the membrane via stretching of the cell wall with a possible coupling of such strains to the cell membrane. The results and analysis presented allow us to conclude on the basis of the experimentally determined breakdown P.K. of 959 mV that the region of membrane where electrical breakdown occurs is a dielectric with one of the following combinations of parameters: (A) a thickness delta=7-9 nm with a dielectric constant epsilon=greater than 10, e.g. a hydrated protein spanning the whole membrane. (B) delta=4-5 nm with epsilon=3-8, e.g. a lipoprotein of lipid bilayer dimensions. (C) delta approximately 2 nm with epsilon=2-3, e.g. a half lipid bilayer. If we assume that the breakdown P.D. of the tonoplast and plasmalemma are identical, that is 480 mV, then there is only one reasonable choice for the membrane thickness and the dielectric constant: delta=2 nm, epsilon=3-8, e.g. a (lipo) proteinaceous module facing a half life lipid bilayer.     

Activation Energy of Nitriding Medium Carbon Ferromanganese Alloy

Investigation of some kinetics aspects of the reaction between nitrogen and medium carbon ferromanganese (MC-FeMn) was made. Nitriding process of fine medium carbon ferromanganese was carried out at temperature ranging from 973 to 1 223 K and time up to 480 min. Nitriding was carried out under nitrogen and hydrogen gas pressures. At temperature of 573 K, hydrogen gas was injected with pressure of about 0.2 MPa followed by injection of nitrogen gas up to 1.2 MPa. Sample mass was 35 g, nitrided in cylindrical chamber with 34 mm in inner diameter and 1 200 mm in length. The change in nitrogen pressure was taken as an indication for nitrogen pickup. The mass gain i.e. nitrogen pickup in kilograms per surface area (m2) was determined by time at different temperatures. Nitriding rate constants were calculated and the activation energy of nitriding process was derived from Arrhenius equation. The nitriding rate constant was found to be increased by increasing temperature of the reaction. The activation energy of nitriding process of fine medium carbon ferromanganese at time ranging up to 28 800 s is around 140 kJ/mol. It was found that the rate controlling step of the nitriding process of MC-FeMn is diffusion mechanism.     

Reduced myocardial Na+, K(+)-pump capacity in congestive heart failure following myocardial infarction in rats

We examined changes in expression and function of the cardiac Na+, K(+)-pump in a post-infarction rat model of hypertrophy and congestive heart failure (CHF). Myocardial infarction was induced by ligation of the left coronary artery in Wistar rats and hearts were obtained from animals with CHF and from sham operated rats after 6 weeks. In the CHF group the ratio of heart weight to body weight was 70% greater compared to sham (*P < 0.05) and all left-ventricular end-diastolic pressures (LVEDP) were above 15 mmHg. The expression of the alpha 1- and beta 1-subunits (mRNA and protein) of the Na+, K(+)-pump was not significantly different in CHF and sham. As compared to sham the alpha 2 isoform, mRNA and protein levels were lower in CHF hearts by 25 and 55%, respectively, whereas the alpha 3 isoform mRNA was greater by 120% in CHF. The alpha 3 protein was not detectable in sham but a prominent band was seen in CHF. Cell volume of isolated cardiomyocytes was 30% larger in CHF. Cardiomyocytes containing the Na+ sensitive fluorescent dye SBFI were loaded to an intracellular Na+ concentration ([Na+]i] of about 140 mM in a K(+)- and Mg(2+)-free medium (140 mM Na+, free Ca2+ of 10(-8) M). To avoid back leak of Na+ and to ensure no voltage effects on the Na+, K(+)-pump extracellular Na+ was subsequently removed, and 6 mM Mg2+ was added to the superfusate, The Na+, K(+)-pump was then reactivated by 10 mM Rb+. SBFI fluorescence ratio decreased mono-exponentially with a time constant (tau) of 191 +/- 15 s in sham (n = 8) and 320 +/- 38 s in CHF (n = 9) rats (P < 0.01). These changes in fluorescence indicate that the maximum rate of decline of [Na+]i from 100 to 35 mM was 39% (P < 0.005) slower in CHF compared to sham, whereas maximum pump rate per cell was not significantly altered (9.0 +/- 0.7 fmol/s in sham and 7.1 +/- 0.7 fmol/s in CHF cells). The [Na+]i which caused 50% pump activation (k0.5) was also not altered in CHF (40 mM in both groups). We conclude that the number of Na+, K(+)-pumps per cell was maintained in CHF but an isoform switch of the alpha 3-replacing the alpha 2-isoform occurred. However, maximum Na+, K(+)-pump rate in terms of rate of change of [Na+]i was significantly attenuated in CHF, most likely as a result of increased cell size.     

高炉块状带压差模型

 高炉上部悬料是高炉生产过程中常见的问题,影响高炉的顺行与高产。块状带压差反映了高炉上部悬料的可能性,更精确地计算块状带压差对高炉生产有重要的指导意义。为了使块状带压差计算结果更符合高炉实际,在原有计算模型的基础上考虑了温度变化影响。基于此模型研究了高压操作与料柱透气性、高炉顺行之间的关系;以迁钢2560m3高炉为例进行计算,计算结果与高炉块状带压差的实测值相符。研究发现：随着顶压的提高,炉料孔隙度、粒径变化对块状带压差的影响幅度越来越小。将该模型应用于处理高炉上部悬料问题时,根据实际炉况计算出在不同顶压下块状带压差随鼓风量的变化曲线,预测操作过程中块状带压差的变化趋势,为定量化处理高炉上部悬料问题提供了参考数据。     

Oxygen tension profiles in isolated hamster retractor muscle at different temperatures

Oxygen tension (P0(2)) profiles within unperfused hamster retractor muscles were obtained at 25, 30, and 37 degrees by using sharpened, recessed oxygen microelectrodes. The microelectrode was driven vertically into freshly excised muscle lying on a flat, impermeable boundary inside a diffusion chamber. Intramuscular P0(2) profiles were measured as a function of electrode depth in 10-mu m steps during both inward and outward penetrations when the upper surface of the muscles was exposed to humidified gases containing 10, 21, 50, and 100% 0(2). The ratio of the 0(2) consumption (M) to the 0(2) permeability (K, Krogh diffusion coefficient = D alpha, diffusion coefficient-solubility product) was estimated by curve-fitting the experimental steady-state distribution of 0(2) through muscles to the analytic solution of the diffusion equation assuming that M obeys zero-order kinetics and K is constant, uniform, and independent of P0(2). The ratios of M/K were independent of temperature and were found to be independent of surface P0(2) and muscle thickness. The average value of M/K was 3.9 +/- 0.45 (SE; n = 30) x 10(5) mm Hg/cm(2), which is consistent with that estimated from previous measurements of M and D using different non-steady-state techniques (Bentley et aL, 1993). These results are consistent with other in vitro 0(2) consumption measurements (Sullivan and Pittman, 1984) and do not provide evidence for nonclassical respiratory activity in resting mammalian skeletal muscle.     

Potassium transport across rabbit descending colon in vitro: evidence for single-file diffusion through a paracellular pathway

The results of previous studies indicate that the bidirectional fluxes of K across short-circuited rabbit descending colon are attributable to passive diffusion through paracellular pathways and that this route is ten times more permeable to K than to Na and Cl. However, transepithelial diffusion potentials in the presence of large transepithelial Na and K concentration differences are much lower than those predicted by the "constant field equation" and appear to be inconsistent with this high K selectivity. The results of the present studies, designed to resolve this apparent contradiction, indicate that: (a) The ratios of the bidirectional transepithelial fluxes of K determined over a wide range of combined chemical and electrical potential differences conform reasonably well with those predicted by the Ussing flux-ratio equation. (b) The permeability coefficient of K (PK), determined from the net fluxes in the presence of concentration differences and from unidirectional fluxes under short-circuit conditions, decreases with increasing K concentration; in the presence of low K concentrations, PK is approximately ten-times PNa, but it approaches PNa in the presence of high K concentrations. PNa is not affected under these conditions. These results provide an explanation for the failure to observe large transepithelial diffusion potentials in the presence of large transepithelial Na and K concentration differences. In addition, these results are consistent with the notion that K diffuses across this preparation through two parallel pathways, one that does not discriminate among K, Na and Cl (a "free-solution" shunt) and another that is highly K selective and involves an interaction with one, or at most two, sites along the route.     

Kinetics of reduction of nickel chloride with hydrogen

The kinetics of reduction of nickel chloride with hydrogen were investigated in the temperature range of 533 (260 °) to 788 K (515 °). Most experiments were done with porous NiCl2 granules having ?8+10 mesh (Tyler) size. The effects of temperature, sample size, granule size and hydrogen partial pressure on the reduction kinetics were investigated. In the temperature range 533 (260 °) to 651 K (378 °) the reduction is dominated by chemical kinetic factors. At higher temperatures diffusional effects appear to become quite significant. The temperature-dependence of the chemical kinetic rate constantK is given by $$\log K = 6.744 - \frac{{22,240}}{{2.303RT}};K\,\,is\,\,in\,\,\min ^{ - 1} $$ The activation energy for the reduction was found to be 22,240 cal /mol (or 93,050 J/mol) in the chemical kinetic regime.