Contribution of Opioid Receptors to the Cytoprotective Effect of the Adaptation to Chronic Hypoxia at Anoxia/Reoxygenation of Isolated Cardiomyocytes

Naryzhnaya, N. V.; Maslov, L. N.; Прокудина, Е С; Lishmanov, Yu. B.

doi:10.1007/s10517-015-2924-7

Cited by 5 publications

(2 citation statements)

References 14 publications

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“…Both effects were mediated via µ- and δ 2 -OR stimulation. We also found that CCH increased tolerance of isolated rat cardiomyocytes to anoxia/reoxygenation [ 61 , 107 ] . The cytoprotective effect of CCH was mediated by µ- and δ 2 -OR activation.…”

Section: The Mechanism Of the Myocardial Ischemic Tolerance Elicited ...mentioning

confidence: 99%

The effect of an adaptation to hypoxia on cardiac tolerance to ischemia/reperfusion

Naryzhnaya¹,

Маслов²,

Derkachev³

et al. 2023

J Biomed Res

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The acute myocardial infarction (AMI) and sudden cardiac death (SCD), both associated with acute cardiac ischemia, are one of the leading causes of adult death in economically developed countries. The development of new approaches for the treatment and prevention of AMI and SCD remains the highest priority for medicine. A study on the cardiovascular effects of chronic hypoxia (CH) may contribute to the development of these methods. Chronic hypoxia exerts both positive and adverse effects. The positive effects are the infarct-reducing, vasoprotective, and antiarrhythmic effects, which can lead to the improvement of cardiac contractility in reperfusion. The adverse effects are pulmonary hypertension and right ventricular hypertrophy. This review presents a comprehensive overview of how CH enhances cardiac tolerance to ischemia/reperfusion. It is an in-depth analysis of the published data on the underlying mechanisms, which can lead to future development of the cardioprotective effect of CH. A better understanding of the CH-activated protective signaling pathways may contribute to new therapeutic approaches in an increase of cardiac tolerance to ischemia/reperfusion.

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Section: The Mechanism Of the Myocardial Ischemic Tolerance Elicited ...mentioning

confidence: 99%

The effect of an adaptation to hypoxia on cardiac tolerance to ischemia/reperfusion

Naryzhnaya¹,

Маслов²,

Derkachev³

et al. 2023

J Biomed Res

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“…CNH not only improves post-ischemic recovery Vol. 68 of heart function , but it also reduces myocardial infarct size (Maslov et al 2013, Chytilova et al 2015, Naryzhnaya et al 2015a and exerts cytoprotective effects against simulated ischemia/reperfusion in isolated cardiomyocytes (Borchert et al 2011, Naryzhnaya et al 2015b.…”

Section: Introductionmentioning

confidence: 99%

Participation of opioid receptors in the cytoprotective effect of chronic normobaric hypoxia

Naryzhnaya

Khaliulin²,

Lishmanov³

et al. 2019

Physiol Res

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We studied the role of the delta, micro, and kappa opioid receptor (OR) subtypes in the cardioprotective effect of chronic continuous normobaric hypoxia (CNH) in the model of acuteanoxia-reoxygenation of isolated cardiomyocytes. Adaptation of rats to CNH was performed by their exposure to atmosphere containing 12% of O(2) for 21 days. Anoxia-reoxygenation of cardiomyocytes isolated from normoxiccontrol rats caused the death of 51 % of cells and lactate dehydrogenase (LDH) release. Adaptation of rats to CNH resulted in the anoxia/reoxygenation-induced cardiomyocyte death of only 38 %, and reduced the LDH release by 25 %. Pre-incubation of the cells with either the non-selective OR (opioid receptor) blocker naloxone (300 nM/l), the delta OR antagonist TIPP(psi) (30 nM/l), the selective delta(2) OR antagonist naltriben (1 nM/l) or the micro OR antagonist CTAP (100 nM/l) for 25 minutes before anoxia abolished the reduction of cell death and LDH release afforded by CNH. The antagonist of delta(1) OR BNTX (1 nM/l) or the kappa OR antagonist nor-binaltorphimine (3 nM/l) did not influence the cytoprotective effects of CNH. Taken together, the cytoprotective effect of CNH is associated with the activation of the delta(2) and micro OR localized on cardiomyocytes.

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Role of ATP-Sensitive K+ Channels in Myocardial Infarct Size-Limiting Effect of Chronic Continuous Normobaric Hypoxia

et al. 2017

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The role of K channels in myocardial infarct size-limiting effect of chronic continuous normobaric hypoxia was examined in a rat model based on a 20-min coronary occlusion and subsequent 3-h reperfusion. Rats were adapted to normobaric hypoxia (12% O) for 21 days. This hypoxia produced a pronounced infarct size-limiting effect, which had been prevented by 0.3 mg/kg glibenclamide, a non-selective inhibitor of entire pool of K channels, or 5 mg/kg 5-hydroxydecanoate, an inhibitor of mitochondrial K channels. The study highlighted the important role of mitochondrial K channels in myocardial infarct size-limiting effect of chronic normobaric hypoxia.

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Contribution of Opioid Receptors to the Cytoprotective Effect of the Adaptation to Chronic Hypoxia at Anoxia/Reoxygenation of Isolated Cardiomyocytes

Cited by 5 publications

References 14 publications

The effect of an adaptation to hypoxia on cardiac tolerance to ischemia/reperfusion

The effect of an adaptation to hypoxia on cardiac tolerance to ischemia/reperfusion

Participation of opioid receptors in the cytoprotective effect of chronic normobaric hypoxia

Role of ATP-Sensitive K+ Channels in Myocardial Infarct Size-Limiting Effect of Chronic Continuous Normobaric Hypoxia

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