Role of endogenous opioid peptides in the infarct size-limiting effect of adaptation to chronic continuous hypoxia

Maslov, L. N.; Нарыжная, Н. В.; Tsibulnikov, S. Yu.; Kolář, František; Zhang, Yi; Wang, Hongxin; Гусакова, А. М.; Lishmanov, Yu. B.

doi:10.1016/j.lfs.2013.07.018

Cited by 52 publications

(65 citation statements)

References 78 publications

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“…Our results are in line with previous reports that demonstrated improved myocardial tolerance to I/R injury in animals adapted to continuous normobaric hypoxia (29,31) or to some regimens of intermittent hypobaric hypoxia corresponding to the altitude of 7,000 m (33) or 5,000 m (48). We also confirmed the recent observation that protective effects do not appear when the hypoxic exposure is interrupted daily with a single brief (60 min) normoxic episode (31).…”

Section: Discussionsupporting

confidence: 93%

Cardioprotective and nonprotective regimens of chronic hypoxia diversely affect the myocardial antioxidant systems

Kasparova

Neckář

Dabrowská

et al. 2015

Physiological Genomics

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Cardioprotective and nonprotective regimens of chronic hypoxia diversely affect the myocardial antioxidant systems. Physiol Genomics 47: 612-620, 2015. First published October 13, 2015; doi:10.1152/physiolgenomics.00058.2015.-It has been documented that adaptation to hypoxia increases myocardial tolerance to ischemia-reperfusion (I/R) injury depending on the regimen of adaptation. Reactive oxygen species (ROS) formed during hypoxia play an important role in the induction of protective cardiac phenotype. On the other hand, the excess of ROS can contribute to tissue damage caused by I/R. Here we investigated the relationship between myocardial tolerance to I/R injury and transcription activity of major antioxidant genes, transcription factors, and oxidative stress in three different regimens of chronic hypoxia. Adult male Wistar rats were exposed to continuous normobaric hypoxia (FIO 2 0.1) either continuously (CNH) or intermittently for 8 h/day (INH8) or 23 h/day (INH23) for 3 wk period. A control group was kept in room air. Myocardial infarct size was assessed in anesthetized open-chest animals subjected to 20 min coronary artery occlusion and 3 h reperfusion. Levels of mRNA transcripts and the ratio of reduced and oxidized glutathione (GSH/GSSG) were analyzed by real-time RT-PCR and by liquid chromatography, respectively. Whereas CNH as well as INH8 decreased infarct size, 1 h daily reoxygenation (INH23) abolished the cardioprotective effect and decreased GSH/GSSG ratio. The majority of mRNAs of antioxidant genes related to mitochondrial antioxidant defense (manganese superoxide dismutase, glutathione reductase, thioredoxin/thioredoxin reductase, and peroxiredoxin 2) were upregulated in both cardioprotective regimens (CNH, INH8). In contrast, INH23 increased only PRX5, which was not sufficient to induce the cardioprotective phenotype. Our results suggest that the increased mitochondrial antioxidant defense plays an important role in cardioprotection afforded by chronic hypoxia. adaptation to hypoxia; cardioprotection; ischemia-reperfusion injury; oxidative stress; antioxidant defense ADAPTATION TO CHRONIC HYPOXIA may improve cardiac tolerance to acute ischemia-reperfusion (I/R) injury under certain conditions. Whereas chronic continuous hypoxia induces a protective cardiac phenotype, a brief daily interruption of hypoxic adaptation for 1 h eliminates the protective effect (31). Tissue damage caused by I/R insult is tightly related to the excess of reactive oxygen species (ROS), but the exact molecular mechanism underlying these adverse effects is still not fully elucidated. Intracellular ROS initiate a sequence of oxidation reactions that can seriously damage cell structures. ROS differ in their reactivity, as well as in mechanisms and sites of their production. These harmful species can be eliminated by specific scavengers. If production of ROS exceeds the capacity limit of antioxidant systems or if the systemic capacity is insufficient, the level of ROS in individual cell compartments increases and generates ...

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Section: Discussionsupporting

confidence: 93%

Cardioprotective and nonprotective regimens of chronic hypoxia diversely affect the myocardial antioxidant systems

Kasparova

Neckář

Dabrowská

et al. 2015

Physiological Genomics

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“…CCNH protective effect was shown previously in the model of the metabolic inhibition of the respiration in isolated CMC [2] and at acute coronary occlusionreperfusion in vivo [6,8]. Moreover, the experiments in vivo revealed the importance of OR in the implementation of the infarct-limiting CCNH effect [6].…”

Section: Resultsmentioning

confidence: 61%

“…L. N. Maslov Adaptation to hypoxia is a promising ways for nondrug improvement of heart tolerance to the effects of ischemia and reperfusion. Thus, the myocardium of animals exposed to chronic continuous normobaric hypoxia (CCNH) becomes resistant to the damaging effects of ischemia and reperfusion [6,8]. However, the mechanism of this effect is still poorly understood.…”

mentioning

confidence: 99%

“…However, the mechanism of this effect is still poorly understood. Infarct size-limiting effect of chronic normobaric hypoxia is implemented via the activation of opioid receptors (OR) [6]. At the same time, exact location of OR mediating the protective effect remains hitherto unclear.…”

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confidence: 99%

“…Intact rats were housed under standard vivarium conditions. Experimental animals were exposed to CCNH at 12% O 2 , 0.3% CO 2 and normal atmospheric pressure for 21 days [6,8]. O 2 and CO 2 pressure inside the hypoxic chamber was constantly maintained by means of BioNova-204G4R1 system (Bio-Nova) and controlled by TCOD-IR and OLC 20 sensors (Oldham) by a controller MX32 (Oldham).…”

mentioning

confidence: 99%

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

et al. 2015

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We examined the role of opioid receptors in the cardioprotective effect of chronic continuous normobaric hypoxia in the model of anoxia/reoxygenation of isolated cardiomyocytes. Adaptation to hypoxia was provided by placing the rats for 21 days in an atmosphere with low O2 content. In intact rats, anoxia/reoxygenation of cardiomyocytes caused death of 23% cells and increased lactate dehydrogenase release from cardiomyocytes. In adapted rats, anoxia/ reoxygenation of cardiomyocytes caused death of only 2.5% cells and the release of lactate dehydrogenase decreased by 25%. Preincubation of the cells with opioid receptor blocker naloxone (300 nM) for 25 min eliminated the adaptive decrease in cell survival and reduction in lactate dehydrogenase release. Hence, opioid receptors of the cardiomyocytes contribute to the cytoprotective effect of chronic normobaric hypoxia.

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Ligand-Directed Signaling at the Delta Opioid Receptor

Vicente-Sánchez

Pradhan

2017

Delta Opioid Receptor Pharmacology and Therapeutic Applications

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Delta opioid receptors (δORs) regulate a number of physiological functions, and agonists for this receptor are being pursued for the treatment of mood disorders, chronic pain, and migraine. A major challenge to the development of these compounds is that, like many G-protein coupled receptors (GPCRs), agonists at the δOR can induce very different signaling and receptor trafficking events. This concept, known as ligand-directed signaling, functional selectivity, or biased agonism, can result in different agonists producing highly distinct behavioral consequences. In this chapter, we highlight the in vitro and in vivo evidence for ligand-directed signaling and trafficking at the δOR. A number of biological implications of agonist-directed signaling at the δOR have been demonstrated. Importantly, ligand-specific effects can impact both acute behavioral effects of delta agonists, as well as the long-term adaptations induced by chronic drug treatment. A better understanding of the specific signaling cascades that regulate these differential behavioral effects would help to guide rational drug design, ultimately resulting in δOR agonists with fewer adverse effects.

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Role of endogenous opioid peptides in the infarct size-limiting effect of adaptation to chronic continuous hypoxia

Cited by 52 publications

References 78 publications

Cardioprotective and nonprotective regimens of chronic hypoxia diversely affect the myocardial antioxidant systems

Cardioprotective and nonprotective regimens of chronic hypoxia diversely affect the myocardial antioxidant systems

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

Ligand-Directed Signaling at the Delta Opioid Receptor

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