Intracellular pH during ischemia in skeletal muscle: relationship to membrane potential, extracellular pH, tissue lactic acid and ATP

1985 ◽  
Vol 404 (4) ◽  
pp. 342-347 ◽  
Author(s):  
Henrik Hagberg
Keyword(s):  
Skeletal Muscle ◽  
Lactic Acid ◽  
Membrane Potential ◽  
Intracellular Ph ◽  
Extracellular Ph

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.

Intracellular pH recovery from lactic acidosis of single skeletal muscle fibres

1988 ◽  
Vol 66 (12) ◽  
pp. 1560-1564 ◽  
Author(s):  
Y. E. Allard
Keyword(s):  
Skeletal Muscle ◽  
Lactic Acid ◽  
Intracellular Ph ◽  
Buffer Capacity ◽  
Ringer Solution ◽  
Sartorius Muscle ◽  
Muscle Fibres ◽  
Diffusion Limited ◽  
Skeletal Muscle Fibres ◽  
Frog Sartorius

Intracellular pH (pHi, measured with H+-selective microelectrodes, in quiescent frog sartorius muscle fibres was 7.29 ± 0.09 (n = 13). Frog muscle fibres were superfused with a modified Ringer solution containing 30 mM HEPES buffer, at extracellular pH (pHo) 7.35. Intracellular pH decreased to 6.45 ± 0.14 (n = 13) following replacement of 30 mM NaCl with sodium lactate (30 mM MES, pHo 6.20). Intracellular pH recovery, upon removal of external lactic acid, depended on the buffer concentration of the modified Ringer solution. The measured values of the pHi recovery rates was 0.06 ± 0.01 ΔpHi/min (n = 5) in 3 mM HEPES and was 0.18 ± 0.06 ΔpHi/min (n = 13) in 30 mM HEPES, pHo 7.35. The Na+–H+ exchange inhibitor amiloride (2 mM) slightly reduced pHi recovery rate. The results indicate that the net proton efflux from lactic acidotic frog skeletal muscle is mainly by lactic acid efflux and is limited by the transmembrane pH gradient which, in turn, depends on the extracellular buffer capacity in the diffusion limited space around the muscle fibres.

scholarly journals Dynamic Changes of Intracellular pH in Individual Lactic Acid Bacterium Cells in Response to a Rapid Drop in Extracellular pH

2000 ◽  
Vol 66 (6) ◽  
pp. 2330-2335 ◽  
Author(s):  
Henrik Siegumfeldt ◽  
K. Björn Rechinger ◽  
Mogens Jakobsen
Keyword(s):  
Lactic Acid ◽  
Lactic Acid Bacteria ◽  
Lactic Acid Bacterium ◽  
Intracellular Ph ◽  
Membrane Filter ◽  
Single Cells ◽  
Streptococcus Thermophilus ◽  
Extracellular Ph ◽  
Lactobacillus Delbrueckii ◽  
Rapid Drop

ABSTRACT We describe the dynamics of changes in the intracellular pH (pHi) values of a number of lactic acid bacteria in response to a rapid drop in the extracellular pH (pHex). Strains of Lactobacillus delbrueckii subsp.bulgaricus, Streptococcus thermophilus, andLactococcus lactis were investigated. Listeria innocua, a gram-positive, non-lactic acid bacterium, was included for comparison. The method which we used was based on fluorescence ratio imaging of single cells, and it was therefore possible to describe variations in pHi within a population. The bacteria were immobilized on a membrane filter, placed in a closed perfusion chamber, and analyzed during a rapid decrease in the pHex from 7.0 to 5.0. Under these conditions, the pHi of L. innocua remained neutral (between 7 and 8). In contrast, the pHi values of all of the strains of lactic acid bacteria investigated decreased to approximately 5.5 as the pHex was decreased. No pronounced differences were observed between cells of the same strain harvested from the exponential and stationary phases. Small differences between species were observed with regard to the initial pHi at pHex 7.0, while different kinetics of pHiregulation were observed in different species and also in different strains of S. thermophilus.

The effect of acid–base changes on skeletal muscle twitch tension

1978 ◽  
Vol 56 (4) ◽  
pp. 543-549 ◽  
Author(s):  
David W. Fretthold ◽  
Lal C. Garg
Keyword(s):  
Carbon Dioxide ◽  
Skeletal Muscle ◽  
Intracellular Ph ◽  
Muscle Tension ◽  
Carbon Dioxide Tension ◽  
Extracellular Ph ◽  
Acid Base ◽  
Muscle Twitch ◽  
Deficient Diet

The effects of acid–base alterations produced by changing bicarbonate (metabolic type), carbon dioxide tension (respiratory type), or both bicarbonate and carbon dioxide tension (compensated type) on skeletal muscle twitch tension, intracellular pH, and intracellular potassium were studied in vitro. Hemidiaphragm muscles from normal rats and rats fed a potassium-deficient diet were used. Decreasing the extracellular pH by decreasing bicarbonate or increasing CO2 in the bathing fluid produced a decrease in intracellular pH, intracellular K+, and muscle twitch tension. However, at a constant extracellular pH, an increase in CO2 (compensated by an increase in bicarbonate) produced an increase in intracellular K+ and twitch tension in spite of a decrease in intracellular pH. The effect on twitch tension of the hemidiaphragms showed a rapid onset, was reversible, persisted until the buffer composition was changed, and was independent of synaptic transmission.It is concluded that the twitch tension of the skeletal muscle decreases with a decrease in intracellular K+. The muscle tension also decreases with an increase in the ratio of intracellular and extracellular H+ concentration. However, there is no consistent relationship between muscle tension and extracellular or intracellular pH. The muscle tension of the diaphragms taken from K+-deficient rats is more sensitive to variations in CO2, pH, and bicarbonate concentration of the medium than that of the control rat diaphragms.

Evidence for altered Na+/H+ antiport activity in cultured skeletal muscle cells and vascular smooth muscle cells from the spontaneously hypertensive rat

1991 ◽  
Vol 80 (5) ◽  
pp. 509-516 ◽  
Author(s):  
J. E. Davies ◽  
L. L. Ng ◽  
M. Ameen ◽  
P. D. Syme ◽  
J. K. Aronson
Keyword(s):  
Skeletal Muscle ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Intracellular Ph ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Extracellular Ph ◽  
Skeletal Muscle Cells ◽  
Spontaneously Hypertensive

1. Intracellular pH and Na+/H+ antiport activity were determined by a fluorimetric method in cultured skeletal muscle cells (myoblasts) and aortic vascular smooth muscle cells from spontaneously hypertensive and normotensive Wistar-Kyoto rats. 2. The intracellular pH was significantly more alkaline at three different extracellular pH values in both myoblasts and vascular smooth muscle cells from the spontaneously hypertensive rats than in those from the normotensive control rats. 3. A kinetic analysis of the Na+/H+ antiport activity in these cells showed that the raised activity in the spontaneously hypertensive rats was due to an increased maximal transport capacity in vascular smooth muscle cells and to an increase in the affinity of the antiport for internal H+ in the myoblasts. 4. When the extracellular pH was reduced in the skeletal muscle cells of both types of rat, the intracellular pH fell. However, in vascular smooth muscle cells, a reduction in the extracellular pH was not associated with a fall in the intracellular pH. This resistance of the intracellular pH to changes in the extracellular pH differentiates vascular smooth muscle cells from other cells that have been studied in this way.

Extracellular acidification at the surface of depolarized voltage-clamped snail neurones detected with eccentric combination pH microelectrodes

1987 ◽  
Vol 65 (5) ◽  
pp. 1001-1005 ◽  
Author(s):  
R. C. Thomas
Keyword(s):  
Membrane Potential ◽  
Intracellular Ph ◽  
Extracellular Ph ◽  
Electrochemical Gradient ◽  
Extracellular Acidification ◽  
Surface Ph ◽  
Buffering Power ◽  
Snail Neurones ◽  
Series Of Experiments ◽  
Ph Microelectrodes

A new design of double micropipette was used to measure intracellular pH, membrane potential, and surface pH of superfused snail neurones. A third double micropipette was used to control the membrane potential via a CsCl-filled barrel and inject HCl iontophoretically. In one series of experiments the surface pH fell by up to one-third of a pH unit when the membrane potential was clamped to 20 mV, pHi was initially 6.7, and extracellular pH was about 7.4 in a medium buffered either with 2 mM HEPES or 2.7% CO2 and 20 mM bicarbonate. In a second series in which surface pH was observed during brief depolarizations to different potentials with different pHi, the potential at which the surface began to acidify varied with pHi with a slope of 32 mV per pH unit. The results confirm that H+ ions leave depolarized snail neurones if the electrochemical gradient is favourable and show that CO2–bicarbonate buffered solutions have a low effective extracellular buffering power for rapid additions of acid.

scholarly journals Changes in Extra- and Intracellular pH in the Brain during and following Ischemia in Hyperglycemic and in Moderately Hypoglycemic Rats

1986 ◽  
Vol 6 (5) ◽  
pp. 574-583 ◽  
Author(s):  
M. -L. Smith ◽  
R. von Hanwehr ◽  
B. K. Siesjö
Keyword(s):  
Lactic Acid ◽  
Intracellular Ph ◽  
Extracellular Ph ◽  
Forebrain Ischemia ◽  
Extracellular Acidosis ◽  
The Brain ◽  
Tissue Metabolites

Incomplete forebrain ischemia of 15-min duration was induced in rats made hyperglycemic or moderately hypoglycemic prior to ischemia. Tissue CO2 tension, CO2 content, labile tissue metabolites, and extracellular pH (pHe) were measured, and intracellular pH (pHi) was derived by calculation on the assumption that cerebral intracellular fluids can be lumped into one space. In hypoglycemic animals, mean tissue lactate content increased from 2 to 10 μmol g−1. Tissue CO2 content was virtually unchanged and the CO2 tension increased from ∼50 to ∼145 mm Hg. In hyperglycemic animals, tissue lactate content rose to 20 μmol g−1, and the CO2 content decreased by 25%, demonstrating that some CO2 was lost to the blood supplied by the remaining perfusion. Accordingly, tissue CO2 tension did not rise above 200 mm Hg. pHe was reduced in proportion to the amount of lactate accumulated, the values obtained in hypo- and hyperglycemic animals showing relatively little scatter (6.76 ± 0.03 and 6.25 ± 0.04, respectively). In hypoglycemic animals the extracellular HCO−3 concentration was virtually unchanged, demonstrating that any influx of lactic acid from the cells must have been accompanied by H+ efflux and/or HCO−3 influx via independent routes. In hyperglycemic animals [HCO−3]e fell by >10 μmol ml−1. In both groups [HCO−3]e was reduced during the first 5 min of recovery. Recovery of pHe was slower in hyper- than in hypoglycemic animals. During ischemia calculated pHi fell to 6.37 ± 0.04 and 5.95 ± 0.06 in hypo- and hyperglycemic animals, respectively. Differences in pHi were maintained for the first 15 min of recovery, but in both hypo- and hyperglycemic animals pHi had normalized after 30 min. It is concluded that preischemic hyperglycemia leads to a more pronounced intra- and extracellular acidosis than normo- and hypoglycemia, an acidosis that also resolves more slowly during recirculation.

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