The effects of external cations and ouabain on the intracellular sodium activity of sheep heart Purkinje fibres

Ellis, David

doi:10.1113/jphysiol.1977.sp012090

Cited by 313 publications

(257 citation statements)

References 40 publications

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“…This software package models the mathematical formalism of the DiFrancesco-Noble description of cardiac currents [149]. By way of verifying the model, DiFrancesco and Noble compared its predictions of intracellular [Na ϩ ] i with those experimentally observed during pump inhibition achieved by the use of ouabain or K ϩ -free solutions [150][151][152]. The model successfully predicted [Na ϩ ] i and, even more impressively, the transient increase of pump current following restoration of [K ϩ ] o .…”

Section: Contributors To the Energymentioning

confidence: 99%

Cardiac Basal Metabolism.

Gibbs

Loiselle²

2001

JJP

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The cardiac basal metabolism is the rate of energy expenditure of the quiescent myocardium. It is also called the resting metabolism or the arrested heart metabolism. It has been measured in numerous ways, and in vivo there is good evidence that it accounts for about 1/5 to 1/3 of the total energy flux. The difficulty arises, however, when the heart is stopped because the magnitude of the basal metabolism depends, as blood viscosity, on how and under what physiological condition it is measured. It is possible for the in vivo basal value to fall to less than 1/5 of its original value without cellular damage or to increase to values 5 times greater than its probable in vivo magnitude (i.e., to rise to values in excess of the energy flux of the normally beating heart) by altering the composition of the perfusion medium. We have written on this subject several times [1][2][3], but believe that developments in knowledge now make it possible for us to speculate in a more informed manner. Since several million openheart operations are performed on arrested hearts worldwide each year, it would seem imperative that we understand the cellular mechanisms that can change the magnitude of basal metabolism.A. V. Hill [4] has pointed out that in examining physiological activities, it is necessary to assume a baseline from which some quantity or rate can be measured. If the energy flux produced by the beating heart were very large compared with the energy flux of the arrested heart, baseline ambiguity would be relatively unimportant. But this is not so in regard to the heart; its basal metabolism is high. Within a species, the basal metabolism of cardiac tissue is several-fold higher than the resting metabolism of skeletal muscle and is an order of magnitude greater than the resting metabolism of amphibian skeletal muscle.Species differences are clearly evident in the magnitude of cardiac basal metabolism, and we believe that the major reason for these differences relates to the leakiness of cell membranes, such as those of the sarcolemma and sarcoplasmic reticulum and those of Japanese Journal of Physiology, 51, 399-426, 2001 Key words: whole hearts, isolated preparations, biochemical contributors, modifiers, species difference, temperature, substrate, hypoxia. Abstract:We endeavor to show that the metabolism of the nonbeating heart can vary over an extreme range: from values approximating those measured in the beating heart to values of only a small fraction of normal-perhaps mimicking the situation of nonflow arrest during cardiac bypass surgery. We discuss some of the technical issues that make it difficult to establish the magnitude of basal metabolism in vivo. We consider some of the likely contributors to its magnitude and point out that the biochemical reasons for a sizable fraction of the heart's basal ATP usage remain unresolved. We consider many of the physiological factors that can alter the basal metabolic rate, stressing the importance of substrate supply. We point out that the protective effect of hypothermia ...

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Section: Contributors To the Energymentioning

confidence: 99%

Cardiac Basal Metabolism.

Gibbs

Loiselle²

2001

JJP

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“…If cardiac glycoside treatment at the mid-neural fold stage of development reduces subsequent neural differentiation because of inhibition of the sodium pump then treatment with potassium-free solution should similarly prevent the development of neurones (see for example, Glynn, 1956;Ellis, 1977). In the whole, punctured embryo it proved impossible to demonstrate an effect of potassium-free solution, almost certainly because leakage of potassium from the cells into the relatively restricted intercellular spaces maintained [K]O sufficiently high to keep the sodium pump activated.…”

Section: Resultsmentioning

confidence: 99%

Intracellular sodium and the differentiation of amphibian embryonic neurones

Breckenridge

Warner

1982

The Journal of Physiology

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SUMMARY1. Experiments have been done to examine the mechanism of the inhibition of neural differentiation produced by inhibiting the sodium pump with cardiac glycosides during the mid-neural fold stages of development of the amphibian embryo. Neural differentiation was assessed quantitatively by counting the number of neurones that undergo primary differentiation in tissue culture, as a proportion of the total number of differentiated cells.2. Inhibition of the sodium pump by lowering the extracellular potassium concentration ([K.]) to 0 during the mid-neural fold stages inhibited neural differentiation.3. Raising the extracellular calcium concentration to 10 mm during treatment with strophanthidin protected differentiating neurones from the effects of the sodium pump inhibitor. Lowering [Ca]o to 0-05 mm potentiated the effect of low doses of glycoside.4. In the presence of high extracellular calcium and 5 x 10-6 M-strophanthidin the membrane potential of neural plate cells remained close to the levels recorded at the beginning of neurulation; the normal increase in resting potential was not restored.5. Addition of 10 mM-Sr2+ to the bathing medium also protected nerve cells against the inhibition produced by strophanthidin; Sr2+ was less effective than Ca2 .6. Addition of either 10 mM-Mg2+ or Mn2+ had no effect on the inhibition of differentiation produced by strophanthidin.7. Addition of Mn2+ along with high Ca2+ prevented calcium from exerting its protective effect. 14. When 10 mM-calcium was present along with strophanthidin [Na]i fell to about 17 mM during neurulation, despite inhibition of the sodium pump. 15. It is concluded that it is unlikely that either abolition of the normal increase in resting potential or a fall in gap junction permeability is responsible for the reduction in neural differentiation produced by blocking the sodium pump during neurulation.16. The results are consistent with the view that strophanthidin achieves its effect by preventing the fall in [Na]i that occurs during normal neurulation because of activation of the sodium pump. They are discussed in the light of this suggestion.

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“…After this the Na activity appears to reach a plateau. In their experiments the activity electrodes were calibrated in a Na solution for which an activity coefficient of 0 75 was assumed (Ellis, 1977). A value of 33-3 mm should reflect the concentration of free ionized intracellular Na in Purkinje fibres under these conditions provided it is assumed that the activity coefficient of the intracellular Na solution is 0 75.…”

Section: Discussionmentioning

confidence: 99%

Sodium efflux in rabbit myocardium: relationship to sodium—calcium exchange

Bridge

Cabeen

Langer

et al. 1981

The Journal of Physiology

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SUMMARY1. The washout of 22Na, 45Ca and 58CoEDTA-has been observed in arterially perfused rabbit interventricular septa both in the presence and absence ofintoxicating doses of the aglycone, 3 acetylstrophanthidin (ACS).2. The washout of 22Na from paced septa (21P0/min) was rapid with approximately 99 % of the exchange occurring in 30 min.3. Septa labelled with 22Na and washed out in the presence of 10-5 M-ACS were quiescent, exhibited marked contracture and a slowed 22Na exchange with 99 % of the initial 22Na leaving the tissue in approximately 200 min.4. Comparison of the washout of the extracellular marker 58CoEDTA-from paced and intoxicated septa revealed no differences, suggesting that regions of the extracellular space had not become inexchangeable as a result of the contracture that these septa exhibited.5. Simultaneous measurements of the distribution of 22Na and 58CoEDTA-in the presence of 10-5 M-ACS revealed an apparent cellular Na concentration of 54-8 + 10-4 (S.E.). This was considerably in excess of the maximum amount of Na contributing to the slowest component of Na efflux from intoxicated septa. Origins of this discrepancy are considered.6. The slowest component of 22Na efflux from intoxicated septa could be markedly stimulated by increasing the external Ca concentration from a nominal 1-5 to 16 mM.The magnitude of stimulation was 44-3 + 7-8 % (S.E.). Increases in the concentration of Mg from 1-0 to 16-0 mm were without effect on the 22Na efflux.7. Application of 10-5 M-ACS produced marked depolarization of the membrane to new stable levels that lay between -10 and -20 mV.8. Washout of ACS after several hours of intoxication resulted in a partial decline in contracture tension, an acceleration of Ca efflux, little change in 22Na efflux and a repolarization of the cell membrane.

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The effects of external cations and ouabain on the intracellular sodium activity of sheep heart Purkinje fibres

Cited by 313 publications

References 40 publications

Cardiac Basal Metabolism.

Cardiac Basal Metabolism.

Intracellular sodium and the differentiation of amphibian embryonic neurones

Sodium efflux in rabbit myocardium: relationship to sodium—calcium exchange

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