The Carbon Dioxide Dissociation Curve of Frog Heart Muscle

Brody, Henry

doi:10.1152/ajplegacy.1930.93.1.190

Cited by 16 publications

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“…There is a large variation in previous estimates of the intracellular buffering capacity of heart muscle. Most of the early work suggested that heart muscle was only poorly buffered in comparison to skeletal muscle (see Brody, 1930) whereas more recently one group have claimed that the reverse is true from in vivo experiments in dog (Clancy & Brown, 1966). They calculated a buffering capacity of about 71 for dog heart.…”

Section: Discussionmentioning

confidence: 99%

Direct measurement of the intracellular pH of mammalian cardiac muscle.

Ellis¹,

Thomas²

1976

The Journal of Physiology

237

109

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SUMMARY1. The intracellular pH (pH,) of sheep heart Purkinje fibres and rat, ferret and guinea-pig ventricle has been measured using recessed-tip pHsensitive micro-electrodes.2. In the absence of CO2 the pHi was approximately 7-2 in all the preparations used. In 5 % CO2 the mean pH, was 7414 in rat and ferret ventricle and 7-02 in sheep Purkinje fibres.3. The pH, response to an increase or a decrease in the CO, level (at constant external pH) was biphasic with a large transient change followed by a partial recovery to a new sustained pH,. 5. The pHi of all the preparations tested indicated that H+ ions were not passively distributed across the cell membrane. There was also little or no pH1 change produced by depolarization with high K solutions.6. Short exposures to hypertonic solutions (100 mm sucrose or 50 mM-KCl) produced a decrease in pHi of approximately 041 pH units.7. Acetazolamide slowed the pHi response to CO2 changes. 8. Restoration of the pHi after displacement by increasing the C02 was not blocked by ouabain or SITS.9. The relationship between pHi and cardiac contractility is discussed.

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Section: Discussionmentioning

confidence: 99%

Direct measurement of the intracellular pH of mammalian cardiac muscle.

Ellis¹,

Thomas²

1976

The Journal of Physiology

237

109

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“…To account for these findings, it has been suggested that pHi is an important controlling factor of cardiac function and falls more during a respiratory than a metabolic acidosis ( 10,26). Though pHi has been measured during a respiratory acidosis in the heart (2,4,9,15,23), there has not been a direct comparison of pHi in metabolic and respiratory acid-base disturbances in muscle from each of the cardiac chambers of a mammal in vivo.…”

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Intracellular pH and K+ of cardiac and skeletal muscle in acidosis and alkalosis

Poole‐Wilson¹,

Ir²

1975

American Journal of Physiology-Legacy Content

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The effects of a metabolic and respiratory acidosis and alkalosis on intracellular pH (pHi) and K+ have been compared in cardiac and skeletal muscle from the anesthetized rabbit. The extracellular space and pHi were calculated from the distribution volumes of [51Cr] EDTA and [14C]DMO, respectively. When pHe was varied by altering PCO2, the slope of the line relating pHi to the extracellular pH (pHe) was greater (P less than 0.05--0.001) than that obtained during metabolic changes of pHe in right and left ventricles, atria, diaphragm, and quadriceps. During metabolic acidosis and alkalosis, the slope of pHi/pHe line did not vary between tissues. During respiratory acidosis, there was no difference in slope between cardiac tissues, but it was less in left ventricle than quadriceps (P less than 0.001). In left ventricle intracellular K+ increased in a metabolic (P less than 0.05) or respiratory acidosis (P less than 0.02), whereas in diaphragm it decreased (P less than 0.02). Intracellular K+ correlated with pHe and pHE-PHi. Changes in pHi but not intracellular K+ could explain known differences in myocardial function in respiratory and metabolic acidosis.

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“…One explanation suggests that hydrogen ions (H + ) and potassium ions (K + ) exchange mole for mole between cells and extracellular fluid during respiratory acid-base disturbances (5). This theory is based on the suggestion that cardiac muscle may not be well buffered (6). Thus, during respiratory acidosis, elevated Pco o will cause a relatively greater increase in [H + ] inside the myocardial cell than it will outside.…”

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Effect of Hypercapnia on Myocardial Potassium Movement in the Dog

Spiker

Smith

1972

Circulation Research

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This investigation tested the hypothesis that uptake of potassium during respiratory acidosis is secondary to the increased catecholamine activity which accompanies hypercapnia. The plasma K + concentration of simultaneously drawn arterial and coronary sinus blood samples from dogs was determined under three conditions: (1) hypercapnia (25% CCv75% O 2 ), (2) normocapnia (25% N 2 -75% O 2 ) + propranolol (a beta-receptor blocker), and (3) hypercapnia + propranolol. The change during hypercapnia from uptake of K + to loss of K + after administration of propranolol (0.05 mg/kg, iv) was statistically significant. However, the administration of propranolol during normocapnia had no effect on myocardial K + movement. Changes in heart rate and myocardial contractility did not explain the change in myocardial K + movement during hypercapnia following the administration of propranolol. These data suggest that uptake of K + is secondary to the increased catecholamine activity which accompanies hypercapnia. KEY WORDSrespiratory acidosis heart potassium propranolol catecholamine beta-receptor blockade• The purpose of this investigation was to study the uptake of potassium by the myocardium during respiratory acidosis (1-4). The mechanism of this movement is not clearly understood. One explanation suggests that hydrogen ions (H + ) and potassium ions (K + ) exchange mole for mole between cells and extracellular fluid during respiratory acid-base disturbances (5). This theory is based on the suggestion that cardiac muscle may not be well buffered (6). Thus, during respiratory acidosis, elevated Pco o will cause a relatively greater increase in [H + ] inside the myocardial cell than it will outside. This proposed simple exchange of H + for K + would, therefore, result in a net uptake of K + by the cardiac muscle cells. This theory can be seriously questioned because recent studies have shown that the buffer capacity of cardiac muscle is greater From the

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The Carbon Dioxide Dissociation Curve of Frog Heart Muscle

Cited by 16 publications

References 0 publications

Direct measurement of the intracellular pH of mammalian cardiac muscle.

Direct measurement of the intracellular pH of mammalian cardiac muscle.

Intracellular pH and K+ of cardiac and skeletal muscle in acidosis and alkalosis

Effect of Hypercapnia on Myocardial Potassium Movement in the Dog

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