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.

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.

pH of isolated resting skeletal muscle and its relation to potassium content

1963 ◽  
Vol 204 (6) ◽  
pp. 1048-1054 ◽  
Author(s):  
Ronald B. Miller ◽  
Ian Tyson ◽  
Arnold S. Relman
Keyword(s):  
Skeletal Muscle ◽  
Intracellular Ph ◽  
Potassium Content ◽  
Ion Concentration ◽  
Detectable Effect ◽  
Rat Diaphragm ◽  
Intracellular Acidosis ◽  
Experimental Conditions ◽  
Hydrogen Ion Concentration

Intracellular pH of isolated rat diaphragm was measured with both a C14-DMO method and a tissue CO2 technique. The values for intracellular pH by each method, although slightly different, changed in parallel under most experimental conditions. Acute, severe potassium depletion in vitro had no detectable effect on intracellular pH, nor did prior depletion in vivo followed by incubation in a potassium-free bath. This was true whether or not the potassium-depleted muscle was exposed to normal or elevated extracellular levels of bicarbonate, and was unaffected by the presence of cationic amino acids in the bath. Acute repletion of previously potassium-depleted muscle resulted in a small rise in cell pH, but this was no greater than that produced by loading normal tissues with potassium. It is concluded that under the conditions of these experiments there is no evidence of intracellular acidosis in potassium-depleted skeletal muscle. Rat diaphragm can lose up to half its potassium content in vitro without detectable increase in hydrogen ion concentration.

Contribution of a net transmembrane HCO3- flux to intracellular acid-base regulation

1977 ◽  
Vol 43 (6) ◽  
pp. 931-935 ◽  
Author(s):  
D. R. Strome ◽  
R. L. Clancy ◽  
N. C. Gonzalez
Keyword(s):  
Carbon Dioxide ◽  
Small Volume ◽  
Elevated Carbon Dioxide ◽  
Ringer Solution ◽  
Carbon Dioxide Tension ◽  
Acid Base ◽  
Initial Cell ◽  
Intracellular Acid

Experiments were performed to determine the relative effects of a net extracellular-to-intracellular HCO3- flux and of elevated carbon dioxide tension (PCO2) on cellular acid-base regulation. Isolated rabbit hearts were perfused by recirculating a small volume of Ringer solution in which the PCO2 and the HCO3- concentration could be independently altered. Net HCO3- flux was assessed by the disappearance of HCO3- from perfusate. Between 40 and 100 Torr PCO2, a HCO3- flux into the cell occurs only when perfusate HCO3- concentration is increased. Therefore, by selective manipulation of perfusate HCO3- and PCO2 it is possible to induce hypercapnia with or without an accompanying HCO3- flux. When perfusate HCO3- concentration was increased from 20 to 36 mM, cellular HCO3- concentration increased from 22.5 +/- 0.8 to 26.1 +/- 1.0 mM at 40 Torr PCO2 and from 27.8 +/- 0.7 to 34.1 +/- 1.4 mM at 98 Torr PCO2. These increases can be accounted for by the amount of HCO3- that disappeared from the perfusate. The results suggest that most of the initial cell CO2 buffering is provided by the net HCO3- flux in addition to the passive physicochemical buffering.

Bicarbonate Therapy and Intracellular Acidosis

1997 ◽  
Vol 93 (6) ◽  
pp. 593-598 ◽  
Author(s):  
D. J. A. Goldsmith ◽  
L. G. Forni ◽  
P. J. Hilton
Keyword(s):  
Carbon Dioxide ◽  
Metabolic Acidosis ◽  
Sodium Bicarbonate ◽  
Intracellular Ph ◽  
Extracellular Fluid ◽  
Intracellular Acidification ◽  
Intracellular Acidosis ◽  
Bicarbonate Therapy ◽  
Intracellular Alkalinization

1. The correction of metabolic acidosis with sodium bicarbonate remains controversial. Experiments in vitro have suggested possible deleterious effects after alkalinization of the extracellular fluid. Disequilibrium of carbon dioxide and bicarbonate across cell membranes after alkali administration, leading to the phenomenon of ‘paradoxical’ intracellular acidosis, has been held responsible for some of these adverse effects. 2. Changes in intracellular pH in suspensions of leucocytes from healthy volunteers were monitored using a fluorescent intracellular dye. The effect in vitro of increasing extracellular pH with sodium bicarbonate was studied at different sodium bicarbonate concentrations. Lactic acid and propionic acid were added to the extracellular buffer to mimic conditions of metabolic acidosis. 3. The addition of a large bolus of sodium bicarbonate caused intracellular acidification as has been observed previously. The extent of the intracellular acidosis was dependent on several factors, being most evident at higher starting intracellular pH. When sodium bicarbonate was added as a series of small boluses the reduction in intracellular pH was small. Under conditions of initial acidosis this was rapidly followed by intracellular alkalinization. 4. Although intracellular acidification occurs after addition of sodium bicarbonate to a suspension of human leucocytes in vitro, the effect is minimal when the conditions approximate those seen in clinical practice. We suggest that the observed small and transient lowering of intracellular pH is insufficient grounds in itself to abandon the use of sodium bicarbonate in human acidosis.

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.

The Acid-Base Status of the Blood of the Developing Chick Embryo

1969 ◽  
Vol 50 (1) ◽  
pp. 79-86
Author(s):  
C. DAWES ◽  
K. SIMKISS
Keyword(s):  
Carbon Dioxide ◽  
Chick Embryo ◽  
Base Excess ◽  
Carbon Dioxide Tension ◽  
Chick Embryos ◽  
Acid Base ◽  
A Value ◽  
Acid Base Status

1. The pH, carbon dioxide tension, bicarbonate and base excess levels of chick embryos have been measured during the period of 11 days of incubation until the 2nd day post hatching. 2. The carbon dioxide tension rises continuously from a value of about 20 mm. Hg on day 11 to a maximum of almost 60 mm. Hg on day 19. 3. The bicarbonate content rises rapidly from the 12th day (16 m-equiv./l.) until the 16th day (33 m-equiv./l.). 4. The pH falls to minimum values on the 13-14th day and the 19th day. 5. These variations are discussed in relation to the physiology of the developing embryo and its acid-base metabolism.

In vitro evidence for sodium-dependent pH regulation in sea lamprey (Petromyzon marinus) red blood cells

1992 ◽  
Vol 70 (3) ◽  
pp. 411-416 ◽  
Author(s):  
Bruce L. Tufts
Keyword(s):  
Carbon Dioxide ◽  
Blood Cells ◽  
Ph Regulation ◽  
Petromyzon Marinus ◽  
Sea Lamprey ◽  
Carbon Dioxide Tension ◽  
Factors Influencing ◽  
Rate Of Increase ◽  
Sodium Dependent

Factors influencing the pH of sea lamprey (Petromyzon marinus) erythrocytes were examined in vitro. The absence of extracellular Na+ caused a significant reduction in the erythrocyte pH. In addition, the protonophore 2,4-dinitrophenol was capable of reducing the erythrocyte pH when it was dissolved in dimethyl sulfoxide. In the presence of ouabain, a step increase in the carbon dioxide tension caused a large increase in the intracellular Na+ concentration, but the rate of increase was considerably reduced after the 1st hour. Even in the absence of ouabain, however, the intracellular Na+ concentration in erythrocytes equilibrated with 3% CO2 is much greater than that in erythrocytes equilibrated with 0.2% CO2. Together, these results suggest that Na+-dependent H+ movements, possibly Na+–H+ exchange, may have an important role in erythrocyte pH regulation in P. marinus. Moreover, the mechanism appears to be stimulated by the decrease in extracellular or erythrocyte pH associated with the increase in [Formula: see text]. Extracellular Na+ also has a significant impact on the CO2-transport properties of P. marinus blood. In the absence of extracellular Na+, the intracellular total CO2 concentration was significantly reduced, whereas extracellular total CO2 concentration, [Formula: see text], was significantly increased. Furthermore, in the no-Na+ saline, [Formula: see text] became dependent on the hematocrit; an increase in the number of erythrocytes resulted in an increase in [Formula: see text]. This result suggests that the erythrocyte membrane of P. marinus may be permeable to [Formula: see text].

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