Advances in Clinical and Experimental Medicine

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Advances in Clinical and Experimental Medicine

2018, vol. 27, nr 8, August, p. 1069–1073

doi: 10.17219/acem/70192

Publication type: original article

Language: English

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Creative Commons BY-NC-ND 3.0 Open Access

Opioidergic conditioning of the human heart muscle in nitric oxide-dependent mechanism

Marcin Kunecki1,A,B,C,D, Tomasz Roleder2,A,B,C, Jolanta Biernat3,C,E,F, Paweł Kukla4,D,E, Lidia Tomkiewicz-Pająk1,C,E,F, Marek A. Deja5,A,E,F, Piotr Podolec1,E,F, Krzysztof S. Gołba3,A,E,F, Wojciech Płazak1,D,E,F

1 Department of Cardiac and Vascular Diseases, the John Paul II Hospital, Jagiellonian University Medical College, Kraków, Poland

2 Department of Cardiology, Medical University of Silesia in Katowice, Poland

3 Department of Electrocardiology and Heart Failure, Medical University of Silesia in Katowice, Poland

4 Faculty of Health Sciences, Jagiellonian University Medical College, Kraków, Poland

5 Department of Cardiac Surgery, Medical University of Silesia in Katowice, Poland

Abstract

Background. Opioidergic conditioning is well documented to trigger cardioprotection against ischemia/ reperfusion (I/R) injury. Previous studies on animal models have suggested that nitric oxide (NO) mediates the beneficial effect of opioids, but the role of NO in humans seems to be controversial.
Objectives. The aim of the study was to assess the influence of NO modulators on opioid-induced cardioprotection in the human myocardium.
Material and Methods. Trabeculae of the human right atria were electrically driven in an organ bath and subjected to simulated I/R injury. The non-selective inhibitor of nitric oxide synthase (NOS) – N-methyl-l-arginine (LNMMA), the donor of NO – S-Nitroso-N-acetylpenicillamine (SNAP) or morphine (in the amount of 10−4 M) were used at the time of re-oxygenation. The additional trabecula was subjected to the hypoxia protocol only (control). The contractility 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 the cardiac muscle relaxation – as the rate of decay of the force of a contraction (Slope T).
Results. The application of 100 μM LNMMA resulted in the decrease of Amax, Slope L and Slope T during the re-oxygenation period as compared to control. The application of 10−4 M morphine and/or 100 μM SNAP resulted in a partial reversal of the detrimental influence of LNMMA.
Conclusion. At the re-oxygenation period, the blockade of NO synthesis has a deleterious effect on the systolic and diastolic function of the human myocardium as well as attenuates the beneficial effect of morphine conditioning.

Key words

ischemia, nitric oxide, reperfusion, morphine

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