Intracellular Buffering in the Dog at Varying CO2 Tensions

1972 ◽  
Vol 42 (3) ◽  
pp. 311-324 ◽  
Author(s):  
J. L. Gamble ◽  
P. J. Zuromskis ◽  
J. A. Bettice ◽  
R. L. Ginsberg
Keyword(s):  
Metabolic Acidosis ◽  
Stroke Volume ◽  
Intracellular Ph ◽  
Concentration Gradient ◽  
Significant Interaction ◽  
Cell Membranes ◽  
Mineral Acid ◽  
Extracellular Ph ◽  
Ion Concentration ◽  
Respiratory Change

1. The effect of varying the Pco2 on the buffering of mineral acid has been investigated. HCl (6 mmol/kg) was infused into anaesthetized-paralysed dogs maintained on a respirator and changes in Pco2 (between 20 and 60 mmHg) were arranged by varying the stroke volume. 2. No significant interaction between buffering of respiratory and metabolic events was discerned. Variations in Pco2 did not alter the efficiency of the buffering of the HCl. The presence or absence of metabolic acidosis did not alter the magnitude of the effect of acute respiratory change on the concentration of extracellular bicarbonate. This response remained between 1·0 and 1·3 mmol/l for changes of 10 mmHg in the Pco2. 3. The buffering of HCl achieved outside the blood and extracellular fluids did not correlate with measured changes in extracellular pH or with predicted changes in intracellular pH. This buffering appears to be associated with changes in the H+ ion concentration gradient across the cell membranes.

Ammonia movement and distribution after exercise across white muscle cell membranes in rainbow trout

1996 ◽  
Vol 271 (3) ◽  
pp. R738-R750 ◽  
Author(s):  
Y. Wang ◽  
G. J. Heigenhauser ◽  
C. M. Wood
Keyword(s):  
Membrane Potential ◽  
Cell Membrane ◽  
Intracellular Ph ◽  
Muscle Cell ◽  
Cell Membranes ◽  
White Muscle ◽  
Extracellular Ph ◽  
Posterior Portion ◽  
Arterial Inflow ◽  
Muscle Cell Membrane

Manipulations of pH and electrical gradients in a perfused preparation were used to analyze the factors controlling ammonia distribution and flux in trout white muscle after exercise. Trout were exercised to exhaustion, and then an isolated-perfused white muscle preparation with discrete arterial inflow and venous outflow was made from the posterior portion of the tail. The tail-trunks were perfused with low (7.4)-, medium (7.9)-, and high (8.4)-pH saline, achieved by varying HCO3- concentration ([HCO3-]) at constant Pco2. Intracellular and extracellular pH, ammonia, CO2, K+, Na+, and Cl- were measured. Muscle intracellular pH was not affected by changes in extracellular pH. Increasing extracellular pH caused a decrease in the transmembrane NH3 partial pressure (PNH3) gradient and a decrease in ammonia efflux. When extracellular K+ concentration was increased from 3.5 to 15 mM in the medium-pH group, a depolarization of the muscle cell membrane potential from -92 to -60 mV and a 0.1-unit depression in intracellular pH occurred. Ammonia efflux increased despite a marked reduction in the PNH3 gradient. Amiloride (10(-4) M) had no effect, indicating that Na+/H(+)-NH4+ exchange does not participate in ammonia transport in this system. A comparison of observed intracellular-to-extracellular ammonia distribution ratios with those modeled according to either pH or Nernst potential distributions supports a model in which ammonia distribution across white muscle cell membranes is affected by both pH and electrical gradients, indicating that the membranes are permeable to both NH3 and NH4+. Membrane potential, acting to retain high levels of NH4+ in the intracellular compartment, appears to have the dominant influence during the postexercise period. However, at rest, the pH gradient may be more important, resulting in much lower intracellular ammonia levels and distribution ratios. We speculate that the muscle cell membrane NH3-to-NH4+ permeability ratio in trout may change between the rest and postexercise condition.

The Effect of Simulated Metabolic Acidosis on Intracellular pH and Lactate Metabolism in the Isolated Perfused Rat Liver

1973 ◽  
Vol 45 (4) ◽  
pp. 543-549 ◽  
Author(s):  
M. H. Lloyd ◽  
R. A. Iles ◽  
B. R. Simpson ◽  
J. M. Strunin ◽  
J. M. Layton ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Intracellular Ph ◽  
Rat Liver ◽  
Extracellular Ph ◽  
Isolated Perfused Rat Liver ◽  
Perfused Rat Liver ◽  
Lactate Metabolism ◽  
Lactate Output ◽  
Lactate Uptake ◽  
The Relationship

1. The relationship between extracellular pH (pHe), intracellular pH (pHi) and lactate uptake was studied in the isolated perfused rat liver during simulated metabolic acidosis. 2. pHi fell to a considerably less extent than pHe when the latter was decreased from pH 7·4 to 6·7. 3. The liver took up lactate when pHi was greater than 7·0; at lower values of pHi lactate output occurred. 4. The relevance of these observations to the control of hepatic pHi and lactate metabolism is discussed.

Plasma, Extracellular and Muscle Electrolyte Responses to Acute Metabolic Acidosis

1956 ◽  
Vol 186 (1) ◽  
pp. 131-138 ◽  
Author(s):  
Richard B. Tobin
Keyword(s):  
Metabolic Acidosis ◽  
Hydrochloric Acid ◽  
Intracellular Ph ◽  
Extracellular Ph ◽  
Acid Base ◽  
Extracellular Acidosis ◽  
Acid Load ◽  
Acute Metabolic Acidosis ◽  
Volumes Of Distribution

Nephrectomized cats were infused with hydrochloric acid in loads of from 3.5–9.6 mEq/kg. Extracellular moderation of the acidosis calculated from concentrations of electrolytes in plasma and inulin volumes of distribution was proportioned as follows: 35% by Na and 5% by K entering the ECS, and 20% by Cl and 24% by CO2 leaving the ECS. Calculated from changes in the chloride spaces, Na shift moderated 58%, CO2 22% and K 6% of the acid load. Sodium rather than potassium appeared to be the main extracellular moderator of acidosis under the conditions of these experiments. Direct muscle analyses showed a fall in intracellular Na and probably of K in response to extracellular acidosis. It is suggested that K i is not inversely related to extracellular ph. Calculated intracellular ph remained constant during the acidosis, indicating that cells may maintain a constant acid-base environment despite marked fluctuations of extracellular ph and that unmeasured mechanisms are responsible.

Effects of Metabolic Alkalosis, Metabolic Acidosis and Uraemia on Whole-Body Intracellular pH in Man

1977 ◽  
Vol 52 (2) ◽  
pp. 125-135 ◽  
Author(s):  
A. Tizianello ◽  
G. De Ferrari ◽  
G. Gurreri ◽  
N. Acquarone
Keyword(s):  
Metabolic Acidosis ◽  
Intracellular Ph ◽  
Metabolic Alkalosis ◽  
Buffer Capacity ◽  
Normal Subjects ◽  
Extracellular Ph ◽  
Whole Body ◽  
Cellular Environment ◽  
Acid Load ◽  
Acute Metabolic Acidosis

1. Whole-body intracellular pH (pH1) was measured by the 14C-labelled DMO method in twenty-four control subjects, eighteen normal subjects with induced acute metabolic alkalosis, ten normal subjects with induced acute metabolic acidosis, twelve normal subjects with chronic acidosis and in fifteen patients with chronic renal insufficiency and acidosis. 2. The change in pH1 per unit change in extracellular pH is significantly larger in acute metabolic alkalosis than in acute metabolic acidosis. In chronic metabolic acidosis, pH1 decreased in proportion to the total amount of ammonium chloride administered; pH1 was normal in patients with uraemic acidosis. 3. These observations confirm the role that tissue buffers play in the protection of the cellular environment in some forms of acidosis. When the acid load overwhelms tissue buffer capacity, pH1 becomes a function of extracellular pH. 4. Cells seem more protected from acute acidosis than from acute alkalosis.

THE EFFECTS OF ELASTIC STIFFENING ON THE EVOLUTION OF THE STRESS FIELD WITHIN A SPHERICAL ELECTRODE PARTICLE OF LITHIUM-ION BATTERIES

2013 ◽  
Vol 05 (04) ◽  
pp. 1350040 ◽  
Author(s):  
WENBIN ZHOU ◽  
FENG HAO ◽  
DAINING FANG
Keyword(s):  
Stress Field ◽  
Lithium Ion Batteries ◽  
Internal Stress ◽  
Concentration Gradient ◽  
Concentration Field ◽  
Lithium Ion ◽  
Coupling Model ◽  
Ion Concentration ◽  
Hysteresis Phenomenon ◽  
Mechanical Coupling

Poor cyclic performance of lithium-ion batteries is calling for efforts to study its capacity attenuation mechanism. The internal stress field produced in the lithium-ion battery during its charging and discharging process is a major factor for its capacity attenuation, research on it appears especially important. We established an electrochemical –mechanical coupling model with the consideration of the influence of elastic stiffening on diffusion for graphite anode materials. The results show that the inner stress field strongly depends on the lithium-ion concentration field, greater concentration gradients lead to greater stresses. The evolution of the stress field is similar to that of the concentration gradient but lags behind it, which shows hysteresis phenomenon. Elastic stiffening can lower the concentration gradient and increase elastic modulus, which are two major factors influencing the inner stress field. We conclude that the latter is more dominant compared to the former, and elastic stiffening acts to increasing the internal stress.

Adaptation to hypercapnia vs. intracellular pH in cat carotid body: responses in vitro

1996 ◽  
Vol 80 (4) ◽  
pp. 1090-1099 ◽  
Author(s):  
S. Lahiri ◽  
R. Iturriaga ◽  
A. Mokashi ◽  
F. Botre ◽  
D. Chugh ◽  
...  
Keyword(s):  
Steady State ◽  
Intracellular Ph ◽  
Baseline Level ◽  
Discharge Rate ◽  
Initial Response ◽  
Extracellular Ph ◽  
Carotid Bodies ◽  
Initial Peak ◽  
Initial Change

The hypotheses that the chemosensory discharge rate parallels the intracellular pH (pHi) during hypercapnia and that the initial change in pHi (delta pHi) is always more than the stead-state delta pHi were studied by using cat carotid bodies in vitro at 36.5 degrees C in the absence and presence of methazolamide (30-100 mg/l). Incremental acidic hypercapnia was followed by an incremental initial peak response and a greater adaptation. A given acidic hypercapnia elicited a rapid initial response followed by a slower adaptation; isohydric hypercapnia produced an equally rapid initial response but of smaller magnitude that returned to near-baseline level; alkaline hypercapnia induced a similar rapid initial response but one of still smaller magnitude that decreased rapidly to below the baseline. Methazolamide eliminated the initial overshoot, which also suggested involvement of the initial rapid pHi in the overshoot. These results show that the initial delta pHi is always greater than the steady-state delta pHi and during hypercapnia. Also, the steady-state chemoreceptor activity varied linearly with the extracellular pH, indicating a linear relationship between extracellular pH and pHi.

Influence of intracellular acidosis on contractile function in the working rat heart

1987 ◽  
Vol 253 (6) ◽  
pp. H1499-H1505 ◽  
Author(s):  
F. M. Jeffrey ◽  
C. R. Malloy ◽  
G. K. Radda
Keyword(s):  
Stroke Volume ◽  
Intracellular Ph ◽  
Rat Heart ◽  
Contractile Function ◽  
High Energy ◽  
Resonance Spectroscopy ◽  
High Energy Phosphates ◽  
Intracellular Acidosis ◽  
Tension Development ◽  
O2 Delivery

The decrease in myocardial contractility during ischemia, hypoxia, and extracellular acidosis has been attributed to intracellular acidosis. Previous studies of the relationship between pH and contractile state have utilized respiratory or metabolic acidosis to alter intracellular pH. We developed a model in the working perfused rat heart to study the effects of intracellular acidosis with normal external pH and optimal O2 delivery. Intracellular pH and high-energy phosphates were monitored by 31P nuclear magnetic resonance spectroscopy. Hearts were perfused to a steady state with a medium containing 10 mM NH4Cl (extracellular pH, 7.4). The subsequent washout of NH3 from the cytosol generated a slight acidosis (from intracellular pH 7.0 to 6.8) which was associated with little change in the determinants of O2 consumption (rate-pressure product) and O2 delivery (coronary flow). Acidosis induced a substantial decrease in aortic flow and stroke volume which was associated with little change in peak systolic pressure. Results were qualitatively similar at different external [Ca2+] (1.75, 2.5, 3.15 mM) and preload (12 or 21 cmH2O) but were most prominent at the lowest external [Ca2+] and left atrial pressure. In contrast to this model of isolated intracellular acidosis, hearts subject to a respiratory (extracellular plus intracellular) acidosis showed a marked reduction in pressure development. It was concluded that 1) for the same intracellular acidosis the influence on tension development was more pronounced with a combined extra- and intracellular acidosis than with an isolated intracellular acidosis, and 2) stroke volume at constant preload was impaired by intracellular acidosis even though changes in developed pressure were minimal. These observations suggest that isolated intracellular acidosis has adverse effects on diastolic compliance and/or relaxation.

Sulfate transport in human lung fibroblasts (IMR-90): effect of pH and anions

1989 ◽  
Vol 256 (3) ◽  
pp. C486-C494 ◽  
Author(s):  
A. Elgavish ◽  
E. Meezan
Keyword(s):  
Intracellular Ph ◽  
Human Lung ◽  
Initial Rate ◽  
Ph Effect ◽  
Kinetic Studies ◽  
Normal Activity ◽  
Extracellular Ph ◽  
Lung Fibroblasts ◽  
Sulfate Transport ◽  
Human Lung Fibroblasts

We previously reported the presence of a carrier-mediated sulfate transport system in human lung fibroblasts (IMR-90) (A. Elgavish, J. B. Smith, D. J. Pillion, and E. Meezan. J. Cell. Physiol. 125: 243-250, 1985). Kinetic studies carried out in the lung fibroblasts show that Cl- inhibits SO4(2-) uptake in a competitive manner. Taken together with the fact that high extracellular Cl- stimulates SO4(2-) efflux, these results suggest that SO4(2-) uptake into lung fibroblasts occurs via a SO4(2-)-Cl- exchange mechanism. Extracellular HCO3- inhibits sulfate influx in a competitive manner (pH 7.5) but has no marked effect on sulfate efflux. SO4(2-) and HCO3- may therefore have the ability to bind to a common extracellular anion binding site, but they do not appear to exchange for one another. Lowering extracellular pH has a stimulatory effect on the initial rate of sulfate uptake. The pK of the extracellular pH effect is around pH 7.0, indicating that small changes in the extracellular pH around the ambient levels encountered under physiological conditions will markedly affect sulfate influx into the cell. Kinetic studies suggest that lowering extracellular pH increases the initial rate of sulfate influx by increasing the affinity of the carrier for sulfate twofold. Lowering intracellular pH inhibits the initial rate of sulfate influx into the cell. The pK of this intracellular pH effect is also around pH 7.0, indicating that physiological levels of intracellular protons are necessary for the normal activity of the anion exchanger.(ABSTRACT TRUNCATED AT 250 WORDS)

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