Effects of acid‐base changes on excitation‐‐contraction coupling in guinea‐pig and rabbit cardiac ventricular muscle.

Fry, Christopher; Poole‐Wilson, P.A.

doi:10.1113/jphysiol.1981.sp013655

Cited by 114 publications

(51 citation statements)

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“…This decrease in phase 2 amplitude of MAP is consistent with previous reports (9,19,20), which has been ascribed to a decrease in plateau-phase Ca 2+ influx (19,21). Meanwhile, with regard to the shortening of MAP duration, some studies reported that a decrease in extracellular pH shortens the action potential duration (22 -25), but the others described opposite results (26,27). It has been reported that under acidic condi- tions, H + directly binds to I Kr and I Ca channels, resulting in their current inhibitions (11,19,20,28).…”

Section: Discussionsupporting

confidence: 80%

Effects of pH on Nifekalant-Induced Electrophysiological Change Assessed in the Langendorff Heart Model of Guinea Pigs

et al. 2014

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Abstract. Since information regarding the effects of pH on the extent of nifekalant-induced repolarization delay and torsades de pointes remains limited, we assessed it with a Langendorff heart model of guinea pigs. First, we investigated the effects of pH change from 7.4 to 6.4 on the bipolar electrogram simulating surface lead II ECG, monophasic action potential (MAP), effective refractory period (ERP), and terminal repolarization period (TRP) and found that acidic condition transiently enhanced the ventricular repolarization. Next, we investigated the effects of pH change from 6.4 to 7.4 in the presence of nifekalant (10 mM) on the ECG, MAP, ERP, TRP, and short-term variability (STV) of MAP 90 and found that the normalization of pH prolonged the MAP 90 and ERP while the TRP remained unchanged, suggesting the increase in electrical vulnerability of the ventricle. Meanwhile, the STV of MAP 90 was the largest at pH 6.4 in the presence of nifekalant, indicating the increase in temporal dispersion of repolarization, which gradually decreased with the return of pH to 7.4. Thus, a recovery period from acidosis might be more dangerous than during the acidosis, because electrical vulnerability may significantly increase for this period while temporal dispersion of repolarization remained increased.

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Section: Discussionsupporting

confidence: 80%

Effects of pH on Nifekalant-Induced Electrophysiological Change Assessed in the Langendorff Heart Model of Guinea Pigs

et al. 2014

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“…Values of pHï and pHé in these solutions are shown in Table 1. Because Ca¥ and HCO×¦ form ion pairs in solution, changes to [NaHCO×] necessitated changes to [CaClµ] in these superfusates to maintain constant the ionized calcium concentration (Fry & Poole-Wilson, 1981). Solutions containing 9·6 and 48 mÒ NaHCO× contained 1·55 and 2·34 mÒ CaClµ, respectively, to maintain the same ionized calcium concentration as was present in Tyrode solution (24 mÒ NaHCO×, 1·8 mÒ CaClµ), and were checked with a Ca¥-selective electrode.…”

Section: Solutionsmentioning

confidence: 99%

The effects of extracellular and intracellular pH on intracellular Ca²⁺ regulation in guinea‐pig detrusor smooth muscle

Fry

1998

The Journal of Physiology

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Intracellular pH (pHi) and intracellular [Ca2+] ([Ca2+]i) were measured during changes to superfusate PCO2 and/or [NaHCO3]. Changes to superfusate PCO2 produced sustained changes to pHi and [Ca2+]i, while changes to [NaHCO3] altered only extracellular pH (pHo). Carbachol or caffeine induced a transient rise of [Ca2+]i due to Ca2+ release from an intracellular store. This Ca2+ transient was reduced by extracellular acidosis, but increased by intracellular acidosis. Alkalosis in either compartment produced opposite effects to acidosis. Changes to the Ca2+ transient mirrored those to phasic tension previously reported in this preparation. A raised superfusate [K+] also induced a Ca2+ transient, due to transmembrane influx of Ca2+. This transient was depressed by extracellular acidosis, but unaffected by changes to pHi. The L‐type Ca2+ current was similarly affected by changes to pHo, but not by alteration of pHi. The results suggest that extracellular acidosis depresses the Ca2+ transient by reducing transmembrane influx through the L‐type Ca2+ channel. The increase in the carbachol‐ and caffeine‐induced Ca2+ transients by intracellular acidosis is due to enhancement of Ca2+ uptake into intracellular stores as a result of a raised resting [Ca2+]i.

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“…This possibility is supported by the present experiments. Although the effects of acidosis on APD in the mammalian heart are controversial (Chesnais et al, 1975;Fry and Poole-Wilson, 1981;Sato et al, 1985;Komukai et al, 2002), we clearly showed a prolongation of the AP at different repolarization times throughout the acidosis period in the toad ventricle. The mechanism of the AP prolongation was not explored in the present work.…”

Section: Dependence Of Contractile Recovery On Ca 2+ Influx: Ncx Vs Lmentioning

confidence: 81%

“…The initial impairment of contractility is followed by a partial recovery that occurs in spite of the persistent extracellular acidosis (Mattiazzi and Cingolani, 1977b;Fry and Poole-Wilson, 1981;Cingolani et al, 1990;Pérez et al, 1993). Considerable research has been done in mammalian heart, in order to elucidate the causes of this recovery (e.g.…”

Section: Introductionmentioning

confidence: 99%

Contractile recovery from acidosis in toad ventricle is independent of intracellular pH and relies upon Ca2+ influx

Salas

Petroff

Venosa

et al. 2006

Journal of Experimental Biology

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SUMMARY Hypercapnic acidosis produces a negative inotropic effect on myocardial contractility followed by a partial recovery that occurs in spite of the persistent extracellular acidosis. The underlying mechanisms of this recovery are far from understood, especially in those species in which excitation–contraction coupling differs from that of the mammalian heart. The main goal of the present experiments was to obtain a better understanding of these mechanisms in the toad heart. Hypercapnic acidosis,induced by switching from a bicarbonate-buffered solution equilibrated with 5%CO2 to the same solution equilibrated with 12% CO2,evoked a decrease in contractility followed by a recovery that reached values higher than controls after 30 min of continued acidosis. This contractile pattern was associated with an initial decrease in intracellular pH(pHi) that recovered to control values in spite of the persistent extracellular acidosis. Blockade of the Na+/H+ exchanger(NHE) with cariporide (5 μmol l–1) produced a complete inhibition of pHi restitution, without affecting the mechanical recovery. Hypercapnic acidosis also produced a gradual increase of diastolic and peak Ca2+i transient values, which occurred immediately after the acidosis was settled and persisted during the mechanical recovery phase. Inhibition of Ca2+ influx through the reverse mode of the Na+/Ca2+ exchanger (NCX) by KB-R (1 μmol l–1 for myocytes and 20 μmol l–1 for ventricular strips), or of L-type Ca2+ channels by nifedipine (0.5μmol l–1), completely abolished the mechanical recovery. Acidosis also produced an increase in the action potential duration. This prolongation persisted throughout the acidosis period. Our results show that in toad ventricular myocardium, acidosis produces a decrease in contractility,due to a decrease in Ca2+ myofilament responsiveness, followed by a contractile recovery, which is independent of pHi recovery and relies on an increase in the influx of Ca2+. The results further indicate that both the reverse mode NCX and the L-type Ca2+channels, appear to be involved in the increase in intracellular Ca2+ concentration that mediates the contractile recovery from acidosis.

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Effects of acid‐base changes on excitation‐‐contraction coupling in guinea‐pig and rabbit cardiac ventricular muscle.

Cited by 114 publications

References 50 publications

Effects of pH on Nifekalant-Induced Electrophysiological Change Assessed in the Langendorff Heart Model of Guinea Pigs

Effects of pH on Nifekalant-Induced Electrophysiological Change Assessed in the Langendorff Heart Model of Guinea Pigs

The effects of extracellular and intracellular pH on intracellular Ca²⁺ regulation in guinea‐pig detrusor smooth muscle

Contractile recovery from acidosis in toad ventricle is independent of intracellular pH and relies upon Ca2+ influx

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Effects of acid‐base changes on excitation‐‐contraction coupling in guinea‐pig and rabbit cardiac ventricular muscle.

Cited by 114 publications

References 50 publications

Effects of pH on Nifekalant-Induced Electrophysiological Change Assessed in the Langendorff Heart Model of Guinea Pigs

Effects of pH on Nifekalant-Induced Electrophysiological Change Assessed in the Langendorff Heart Model of Guinea Pigs

The effects of extracellular and intracellular pH on intracellular Ca2+ regulation in guinea‐pig detrusor smooth muscle

Contractile recovery from acidosis in toad ventricle is independent of intracellular pH and relies upon Ca2+ influx

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The effects of extracellular and intracellular pH on intracellular Ca²⁺ regulation in guinea‐pig detrusor smooth muscle