open access

Vol 24, No 4 (2017)
Original articles — Basic science and experimental cardiology
Published online: 2016-10-11
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‘Opioidergic postconditioning’ of heart muscle during ischemia/reperfusion injury

Marcin Kunecki, Wojciech Płazak, Tomasz Roleder, Jolanta Biernat, Tomasz Oleksy, Piotr Podolec, Krzysztof S. Gołba
DOI: 10.5603/CJ.a2016.0090
·
Pubmed: 27734456
·
Cardiol J 2017;24(4):419-426.

open access

Vol 24, No 4 (2017)
Original articles — Basic science and experimental cardiology
Published online: 2016-10-11

Abstract

Background: Ischemic preconditioning and postconditioning are the novel strategies of attaining cardioprotection against ischemia/reperfusion (I/R) injury. Previous studies suggested the role of opioid pathway, however the class of opioid receptors responsible for this effect in humans remains unknown. The aim of the study was to assess the influence of opioids on simulated I/R injury outcomes in the hu­man myocardium.

Methods: Trabeculae of the human right atrium were electrically driven in organ bath and subjected to simulated I/R injury. Morphine (10–4M, 10–5M, 10–6M) or d-opioid receptor agonist DADLE (10–8M, 10–7M, 10–6M) was used at the time of re-oxygenation. Additional trabecula was subjected to hypoxia protocol only (Control). Contractive force of the myocardium was assessed as the maximal force of a contraction (Amax), the rate of rise of the force of a contraction (Slope L) and relaxation as the rate of decay of the force of a contraction (Slope T).

Results: Application of morphine 10–4M resulted in increase of Amax, Slope L and Slope T during re-oxygenation period as compared to Control (77.99 ± 1.5% vs. 68.8 ± 2.2%, p < 0.05; 45.72 ± 2.9% vs. 34.12 ± 5.1%, p < 0.05; 40.95 ± 2.5% vs. 32.37 ± 4.3%, p < 0.05). Parameters were not significantly different in the lower morphine concentrations. Application of DADLE 10–6M resulted in decrease of Amax and Slope L as compared to Control (68.13 ± 5.5% vs. 76.62 ± 6.6%, p < 0.05; 28.29 ± 2.2 vs. 34.80 ± 3.9%, p < 0.05).

Conclusions: At re-oxygenation, morphine improves systolic and diastolic function of the human myo­cardium in the dose-dependent manner. Delta-opioid receptor stimulation attenuates systolic function of human heart muscle which remains in contrast to previous reports with animal models of I/R injury. (Cardiol J 2017; 24, 4: 419–425)

Abstract

Background: Ischemic preconditioning and postconditioning are the novel strategies of attaining cardioprotection against ischemia/reperfusion (I/R) injury. Previous studies suggested the role of opioid pathway, however the class of opioid receptors responsible for this effect in humans remains unknown. The aim of the study was to assess the influence of opioids on simulated I/R injury outcomes in the hu­man myocardium.

Methods: Trabeculae of the human right atrium were electrically driven in organ bath and subjected to simulated I/R injury. Morphine (10–4M, 10–5M, 10–6M) or d-opioid receptor agonist DADLE (10–8M, 10–7M, 10–6M) was used at the time of re-oxygenation. Additional trabecula was subjected to hypoxia protocol only (Control). Contractive force of the myocardium was assessed as the maximal force of a contraction (Amax), the rate of rise of the force of a contraction (Slope L) and relaxation as the rate of decay of the force of a contraction (Slope T).

Results: Application of morphine 10–4M resulted in increase of Amax, Slope L and Slope T during re-oxygenation period as compared to Control (77.99 ± 1.5% vs. 68.8 ± 2.2%, p < 0.05; 45.72 ± 2.9% vs. 34.12 ± 5.1%, p < 0.05; 40.95 ± 2.5% vs. 32.37 ± 4.3%, p < 0.05). Parameters were not significantly different in the lower morphine concentrations. Application of DADLE 10–6M resulted in decrease of Amax and Slope L as compared to Control (68.13 ± 5.5% vs. 76.62 ± 6.6%, p < 0.05; 28.29 ± 2.2 vs. 34.80 ± 3.9%, p < 0.05).

Conclusions: At re-oxygenation, morphine improves systolic and diastolic function of the human myo­cardium in the dose-dependent manner. Delta-opioid receptor stimulation attenuates systolic function of human heart muscle which remains in contrast to previous reports with animal models of I/R injury. (Cardiol J 2017; 24, 4: 419–425)

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Keywords

ischemia reperfusion injury, postconditioning, opioids

About this article
Title

‘Opioidergic postconditioning’ of heart muscle during ischemia/reperfusion injury

Journal

Cardiology Journal

Issue

Vol 24, No 4 (2017)

Pages

419-426

Published online

2016-10-11

DOI

10.5603/CJ.a2016.0090

Pubmed

27734456

Bibliographic record

Cardiol J 2017;24(4):419-426.

Keywords

ischemia reperfusion injury
postconditioning
opioids

Authors

Marcin Kunecki
Wojciech Płazak
Tomasz Roleder
Jolanta Biernat
Tomasz Oleksy
Piotr Podolec
Krzysztof S. Gołba

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