Intracellular pH and surface pH in skeletal and cardiac muscle measured with a double-barrelled pH microelectrode

Hemptinne, Alexandre de

doi:10.1007/bf00584198

Cited by 49 publications

(23 citation statements)

References 4 publications

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“…Control values of pH, were found to be similar to those reported by other investigators (26)(27)(28) and were higher than would be predicted from simple passive distribution resulting from the electrochemical gradient across the cell membrane. This transsarcolemmal proton gradient is maintained primarily by Na-H exchange, although there remains some controversy regarding the relative importance of the Cl-HCO3 transport mechanism (29).…”

Section: Methodssupporting

confidence: 86%

Relationship between ionic perturbations and electrophysiologic changes in a canine Purkinje fiber model of ischemia and reperfusion.

Yee¹,

Brown²,

Bolster³

et al. 1988

J. Clin. Invest.

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Standard and ion-sensitive microelectrodes were used to identify the basis of electrophysiologic changes that occur in canine cardiac Purkinje fibers superfused with "ischemic" solution (40 min) and then returned to standard Tyrode's solution. Maximum diastolic potential (EMDP) decreased (-92.6±2.4 to -86.0±4.0 mV; n = 19; P < 0.001) during exposure to "ischemia," and after reperfusion, rapidly hyperpolarized to -90.0±4.7 (2 min) and then depolarized to -47.0±7.5 mV (10 mnu; P < 0.001). No significant change in intracellular K activity (ak) was noted throughout. Extracellular K activity (ak) changed only during reperfusion, reaching a nadir at 5 mmi (3.5±0.4 to 2.6±0.5 mM, P < 0.03), and thus can not account for the decrease in EMDP during reperfusion. Mean aON. increased (8.7±1.3 to 10.9±1.9 mM; n = 10; P < 0.01) during ischemia, but rapidly declined during reperfusion to 5.1±2.2 mM (10 min; P < 0.01). Exposure to acetylstrophanthidin (4-5 X 10-' M) during the final 10 min of ischemia increased aON, to 19.9±3.8 mM (a = 5), which was unchanged at 5 min of reperfusion. This suggests that Na-K pump inhibition during ischemia was minimal and that the pump was stimulated early during reperfusion, accounting for the initial transient hyperpolarization. Resting tension did not change significantly during exposure to ischemia; however, return to control Tyrode's solution caused a marked rise to 11.3±9.9 mg/mm2 (a = 13, P < 0.001). This is consistent with a calcium overload state during reperfusion. The depolarization seen during reperfusion may result from activation of a Ca-activated, nonselective cation channel or enhanced electrogenic Na/Ca exchange.

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Section: Methodssupporting

confidence: 86%

Relationship between ionic perturbations and electrophysiologic changes in a canine Purkinje fiber model of ischemia and reperfusion.

Yee¹,

Brown²,

Bolster³

et al. 1988

J. Clin. Invest.

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“…Earlier, Furusawa & Kerridge (1927) had measured the pH of cell homogenates and suggested that cat uterine muscle was considerably more alkaline than either cardiac or skeletal muscle. Their method was obviously crude, yet their values for skeletal and cardiac muscle are remarkably similar to those obtained since by direct measurement with pH-sensitive micro-electrodes (Ellis & Thomas, 1976a, b;Aickin & Thomas, 1977a;Vaughan-Jones, 1979;de Hemptinne, 1980). pH-sensitive micro-electrodes clearly can provide the most trustworthy measurements and, in addition, enable continuous recording ofchanges in pHi.…”

Section: Intracellular Ph (Phi) Of the Surface Cells Of Guinea-pig Vamentioning

confidence: 62%

“…The value has been used in the following paper (Aickin & Brading, 1984) where it is notable that the conclusions agree with the assumption of such a low value. (Ellis & Thomas, 1976a, b), 7 09 (Vaughan-Jones, 1979) and 7-1-7-2 (de Hemptinne, 1980) in sheep heart Purkinje fibres, and 7 07 (Aickin & Thomas, 1977 a) and7-1-7-2 (de Hemptinne, 1980) in mouse and rat soleus muscle. The similarity between the muscle types extends to their response to changes in pHo at constant CO2, although the resultant changes in pH, occurred faster in smooth muscle, presumably reflecting the larger surface area to volume ratio of these cells.…”

Section: Calculation Of Intracellular Buffering Powermentioning

confidence: 98%

Direct measurement of intracellular pH and buffering power in smooth muscle cells of guinea‐pig vas deferens.

Aickin¹

1984

The Journal of Physiology

120

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SUMMARY1. A double-barrelled, pH-sensitive micro-electrode suitable for use in mammalian smooth muscle has been developed. It was shown to be unaffected by alteration of Na, K, Ca, Mg, Cl or C02, and yielded the same results in mouse soleus muscle as had been obtained previously with the recessed-tip pH-sensitive glass electrode (Aickin & Thomas, 1977a 3. Alteration of extracellular pH (pHO) at constant CO2 caused a smaller change in pHi, by about 40 % of that in pH0. The change was complete in 6-12 min and was of a similar magnitude whether the alteration was made in the continual presence or absence of CO2.4. Alteration of the CO2 level at constant pHo caused a rapid change in pHi followed by a slower, complete recovery. Thus the same stabilized pHi was recorded in different C02-containing solutions. When CO2 was removed, the expected intracellular alkalinization was reduced or even obscured by a considerable acidification.pHi then stabilized at a mean value of 6-81 + 011 (n = 18) with an Em of -60-8 + 8&2 mV. The acidification expected on readmission of CO2 was minimized or obscured by a rapid recovery of pHi to the value previously recorded in C02-containing solutions.5. A simultaneous increase in CO2 and decrease in pHo caused a rapid fall in pHi which increased in magnitude with decreasing pH0. This fall was followed by an incomplete recovery when pHo was above about 6-8 (but below 7 35), by no further change in pHi when pHo was about 6-7 and by a slow, continued fall in pHi when pHo was below 6'7.6. The intrinsic buffering power was calculated from the pHi changes observed on alteration of CO2. The values obtained increased in parallel with the extent to which pHi recovered following the imposed change, probably explained by an inseparable contribution to the minimization of the change by transport processes. It is concluded that the intrinsic buffering power is low and a mean value of 86 + 4-9 mequiv H+ ions/pH unit . (n = 39) is suggested to be the most reliable estimate.7. The similarities and differences between pH, in mammalian smooth, cardiac and skeletal muscle are discussed.

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“…For instance, interstitial acidification at lower buffer concentrations16 may not only reduce arrhythmias by slowing Na+-H+ exchange7; protons also compete with Na+ and Ca 2 for access to their voltage-gated channels. [17][18] Similarly, the antiarrhythmic actions of DMA and HMA need not exclusively be due to inhibition of sarcolemmal Na+-H+ exchange. With prolonged (>5 minutes) exposure, these compounds also have progressive negative chronotropic and vasoconstricting effects (data not shown), which are presumably the result of H+ retention in nodal tissue18 and/or blood vessel walls.…”

Section: Buffering Capacity and Reperfusion Arrhythmiasmentioning

confidence: 99%

Effects of proton buffering and of amiloride derivatives on reperfusion arrhythmias in isolated rat hearts. Possible evidence for an arrhythmogenic role of Na(+)-H+ exchange.

Dennis

Coetzee

Cragoe

et al. 1990

Circulation Research

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Intracellular pH and surface pH in skeletal and cardiac muscle measured with a double-barrelled pH microelectrode

Cited by 49 publications

References 4 publications

Relationship between ionic perturbations and electrophysiologic changes in a canine Purkinje fiber model of ischemia and reperfusion.

Relationship between ionic perturbations and electrophysiologic changes in a canine Purkinje fiber model of ischemia and reperfusion.

Direct measurement of intracellular pH and buffering power in smooth muscle cells of guinea‐pig vas deferens.

Effects of proton buffering and of amiloride derivatives on reperfusion arrhythmias in isolated rat hearts. Possible evidence for an arrhythmogenic role of Na(+)-H+ exchange.

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