Temperature modulates calcium homeostasis and ventricular arrhythmias in myocardial preparations

Giovanni Gambassi, Elisabetta Cerbai, Marco Pahor, Maurizio C. Capogrossi, Pierugo Carbonin, Alessandro Mugelli

Research output: Contribution to journalArticle

Abstract

Objective: The aim was to evaluate the effect of temperature on reoxygenation induced ventricular arrhythmias in isolated hearts, on delayed afterdepolarisations and Iti current in Purkinje fibres, and on sarcoplasmic reticular function and Ca2+ handling of single cardiac myocytes. Methods: Isolated guinea pig hearts were retrogradely perfused at 37°C with a hypoxic medium for 15 min and reoxygenated for 10 min either at 33°C or at 37°C. Intracellular microelectrodes were used to assess the presence of delayed afterdepolarisations and triggered activity in sheep Purkinje fibres exposed to strophanthidin at different temperatures. Iti current was evaluated in voltage clamp experiments. In rat cardiomyocytes, loaded with the fluorescent Ca2+ dye, indo-1, the sarcoplasmic reticular Ca2+ content was assessed at 30°C and at 37°C, either by a caffeine spritz puffed onto a cell from a patch pipette or by a post-rest contraction. Results: Hypothermic reoxygenation reduced the incidence of ventricular arrhythmias in isolated hearts (30%, n = 10, at 33°C and 75%, n = 30, at 37°C, p <0.05). In Purkinje fibres, hypothermia decreased the amplitude of delayed afterdepolarisations. Moreover, at 32°C, the amplitude of Iti current was decreased to 59.2(SEM 2.6)% of the normothermic value [27.5(6.7) nA, n=4, p <0.005] and time to peak increased to 159.7(10.2)% [value at 37°C = 470(41) ms, n=4, p <0.01]. In cardiac cells, sarcoplasmic reticular Ca2+ release induced by caffeine spritz or by post-rest contraction was increased at 30°C. However, following a pacing period at 1 Hz, hypothermia prolonged the time to onset of the first spontaneous Ca2+ oscillation [59(14) s at 30°C and 27(9) s at 37°C, n = 5, p <0.05] and reduced the oscillation frequency [1.1(0.4) min-1 at 30°C and 3.1(0.9) min-1 at 37°C, n = 5, p <0.05]. Conclusions: Mild hypothermia increases sarcoplasmic reticular Ca2+ content but decreases the likelihood of spontaneous Ca2+ release. This may explain the reduction of delayed afterdepolarisations and Iti current amplitude in Purkinje fibres and it could represent a mechanism for the protection provided by hypothermia against ventricular arrhythmias.

Original languageEnglish
Pages (from-to)391-399
Number of pages9
JournalCardiovascular Research
Volume28
Issue number3
Publication statusPublished - Mar 1994

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Hypothermia
Ventricular Arrhythmias
Purkinje Fibers
Homeostasis
Calcium
Cardiac Arrhythmias
Preparation
Caffeine
Temperature
Fibers
Cardiac Myocytes
Fiber
Strophanthidin
Microelectrodes
Clamping devices
Fluorescent Dyes
Contraction
Rats
Sheep
Guinea Pigs

Keywords

  • Ca
  • cardiac myocytes
  • delayed afterdepolarisations: I current, arrhythmias
  • heart
  • reoxygenation
  • sarcoplasmic reticulum
  • temperature

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Statistics, Probability and Uncertainty
  • Applied Mathematics
  • Physiology (medical)
  • Physiology

Cite this

Gambassi, G., Cerbai, E., Pahor, M., Capogrossi, M. C., Carbonin, P., & Mugelli, A. (1994). Temperature modulates calcium homeostasis and ventricular arrhythmias in myocardial preparations. Cardiovascular Research, 28(3), 391-399.

Temperature modulates calcium homeostasis and ventricular arrhythmias in myocardial preparations. / Gambassi, Giovanni; Cerbai, Elisabetta; Pahor, Marco; Capogrossi, Maurizio C.; Carbonin, Pierugo; Mugelli, Alessandro.

In: Cardiovascular Research, Vol. 28, No. 3, 03.1994, p. 391-399.

Research output: Contribution to journalArticle

Gambassi, G, Cerbai, E, Pahor, M, Capogrossi, MC, Carbonin, P & Mugelli, A 1994, 'Temperature modulates calcium homeostasis and ventricular arrhythmias in myocardial preparations', Cardiovascular Research, vol. 28, no. 3, pp. 391-399.
Gambassi G, Cerbai E, Pahor M, Capogrossi MC, Carbonin P, Mugelli A. Temperature modulates calcium homeostasis and ventricular arrhythmias in myocardial preparations. Cardiovascular Research. 1994 Mar;28(3):391-399.
Gambassi, Giovanni ; Cerbai, Elisabetta ; Pahor, Marco ; Capogrossi, Maurizio C. ; Carbonin, Pierugo ; Mugelli, Alessandro. / Temperature modulates calcium homeostasis and ventricular arrhythmias in myocardial preparations. In: Cardiovascular Research. 1994 ; Vol. 28, No. 3. pp. 391-399.
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abstract = "Objective: The aim was to evaluate the effect of temperature on reoxygenation induced ventricular arrhythmias in isolated hearts, on delayed afterdepolarisations and Iti current in Purkinje fibres, and on sarcoplasmic reticular function and Ca2+ handling of single cardiac myocytes. Methods: Isolated guinea pig hearts were retrogradely perfused at 37°C with a hypoxic medium for 15 min and reoxygenated for 10 min either at 33°C or at 37°C. Intracellular microelectrodes were used to assess the presence of delayed afterdepolarisations and triggered activity in sheep Purkinje fibres exposed to strophanthidin at different temperatures. Iti current was evaluated in voltage clamp experiments. In rat cardiomyocytes, loaded with the fluorescent Ca2+ dye, indo-1, the sarcoplasmic reticular Ca2+ content was assessed at 30°C and at 37°C, either by a caffeine spritz puffed onto a cell from a patch pipette or by a post-rest contraction. Results: Hypothermic reoxygenation reduced the incidence of ventricular arrhythmias in isolated hearts (30{\%}, n = 10, at 33°C and 75{\%}, n = 30, at 37°C, p <0.05). In Purkinje fibres, hypothermia decreased the amplitude of delayed afterdepolarisations. Moreover, at 32°C, the amplitude of Iti current was decreased to 59.2(SEM 2.6){\%} of the normothermic value [27.5(6.7) nA, n=4, p <0.005] and time to peak increased to 159.7(10.2){\%} [value at 37°C = 470(41) ms, n=4, p <0.01]. In cardiac cells, sarcoplasmic reticular Ca2+ release induced by caffeine spritz or by post-rest contraction was increased at 30°C. However, following a pacing period at 1 Hz, hypothermia prolonged the time to onset of the first spontaneous Ca2+ oscillation [59(14) s at 30°C and 27(9) s at 37°C, n = 5, p <0.05] and reduced the oscillation frequency [1.1(0.4) min-1 at 30°C and 3.1(0.9) min-1 at 37°C, n = 5, p <0.05]. Conclusions: Mild hypothermia increases sarcoplasmic reticular Ca2+ content but decreases the likelihood of spontaneous Ca2+ release. This may explain the reduction of delayed afterdepolarisations and Iti current amplitude in Purkinje fibres and it could represent a mechanism for the protection provided by hypothermia against ventricular arrhythmias.",
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AU - Cerbai, Elisabetta

AU - Pahor, Marco

AU - Capogrossi, Maurizio C.

AU - Carbonin, Pierugo

AU - Mugelli, Alessandro

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N2 - Objective: The aim was to evaluate the effect of temperature on reoxygenation induced ventricular arrhythmias in isolated hearts, on delayed afterdepolarisations and Iti current in Purkinje fibres, and on sarcoplasmic reticular function and Ca2+ handling of single cardiac myocytes. Methods: Isolated guinea pig hearts were retrogradely perfused at 37°C with a hypoxic medium for 15 min and reoxygenated for 10 min either at 33°C or at 37°C. Intracellular microelectrodes were used to assess the presence of delayed afterdepolarisations and triggered activity in sheep Purkinje fibres exposed to strophanthidin at different temperatures. Iti current was evaluated in voltage clamp experiments. In rat cardiomyocytes, loaded with the fluorescent Ca2+ dye, indo-1, the sarcoplasmic reticular Ca2+ content was assessed at 30°C and at 37°C, either by a caffeine spritz puffed onto a cell from a patch pipette or by a post-rest contraction. Results: Hypothermic reoxygenation reduced the incidence of ventricular arrhythmias in isolated hearts (30%, n = 10, at 33°C and 75%, n = 30, at 37°C, p <0.05). In Purkinje fibres, hypothermia decreased the amplitude of delayed afterdepolarisations. Moreover, at 32°C, the amplitude of Iti current was decreased to 59.2(SEM 2.6)% of the normothermic value [27.5(6.7) nA, n=4, p <0.005] and time to peak increased to 159.7(10.2)% [value at 37°C = 470(41) ms, n=4, p <0.01]. In cardiac cells, sarcoplasmic reticular Ca2+ release induced by caffeine spritz or by post-rest contraction was increased at 30°C. However, following a pacing period at 1 Hz, hypothermia prolonged the time to onset of the first spontaneous Ca2+ oscillation [59(14) s at 30°C and 27(9) s at 37°C, n = 5, p <0.05] and reduced the oscillation frequency [1.1(0.4) min-1 at 30°C and 3.1(0.9) min-1 at 37°C, n = 5, p <0.05]. Conclusions: Mild hypothermia increases sarcoplasmic reticular Ca2+ content but decreases the likelihood of spontaneous Ca2+ release. This may explain the reduction of delayed afterdepolarisations and Iti current amplitude in Purkinje fibres and it could represent a mechanism for the protection provided by hypothermia against ventricular arrhythmias.

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