Sevoflurane induces cardioprotection through reactive oxygen species-mediated upregulation of autophagy in isolated guinea pig hearts

Shiomi, Mayumi; Miyamae, Masami; Takemura, Genzou; Kaneda, Kazuhiro; Inamura, Yoshitaka; Onishi, Anna; Koshinuma, Shizuka; Momota, Yoshihiro; Minami, Toshiaki; Figueredo, Vincent M.

doi:10.1007/s00540-013-1755-9

Cited by 35 publications

(20 citation statements)

References 32 publications

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“…IPC is accomplished through short intermittent bouts of I/R, typically one to five cycles, that leads to endogenous protection against an ensuing longer duration ischemia (Murry et al, 1986). Since then, several pathways leading to cardioprotection have been proposed, but a central theme that has been a mainstay in the IPC literature is that ROS play an intricate role in the cardioprotective signaling mechanisms (Shiomi et al, 2013). The beneficial effects of IPC include a reduction in myocardial infarction (Murry et al, 1986), reperfusion arrhythmias (Shiki and Hearse, 1987), stunning (Bolli et al, 1997), and necrotic and apoptotic cell death (Nakamura et al, 2000).…”

Section: Role Of Ros In Cardiac Preconditioningmentioning

confidence: 99%

The â€œGoldilocks Zoneâ€ from a redox perspectiveâ€”Adaptive vs. deleterious responses to oxidative stress in striated muscle

et al. 2014

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Consequences of oxidative stress may be beneficial or detrimental in physiological systems. An organ system's position on the “hormetic curve” is governed by the source and temporality of reactive oxygen species (ROS) production, proximity of ROS to moieties most susceptible to damage, and the capacity of the endogenous cellular ROS scavenging mechanisms. Most importantly, the resilience of the tissue (the capacity to recover from damage) is a decisive factor, and this is reflected in the disparate response to ROS in cardiac and skeletal muscle. In myocytes, a high oxidative capacity invariably results in a significant ROS burden which in homeostasis, is rapidly neutralized by the robust antioxidant network. The up-regulation of key pathways in the antioxidant network is a central component of the hormetic response to ROS. Despite such adaptations, persistent oxidative stress over an extended time-frame (e.g., months to years) inevitably leads to cumulative damages, maladaptation and ultimately the pathogenesis of chronic diseases. Indeed, persistent oxidative stress in heart and skeletal muscle has been repeatedly demonstrated to have causal roles in the etiology of heart disease and insulin resistance, respectively. Deciphering the mechanisms that underlie the divergence between adaptive and maladaptive responses to oxidative stress remains an active area of research for basic scientists and clinicians alike, as this would undoubtedly lead to novel therapeutic approaches. Here, we provide an overview of major types of ROS in striated muscle and the divergent adaptations that occur in response to them. Emphasis is placed on highlighting newly uncovered areas of research on this topic, with particular focus on the mitochondria, and the diverging roles that ROS play in muscle health (e.g., exercise or preconditioning) and disease (e.g., cardiomyopathy, ischemia, metabolic syndrome).

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Section: Role Of Ros In Cardiac Preconditioningmentioning

confidence: 99%

The â€œGoldilocks Zoneâ€ from a redox perspectiveâ€”Adaptive vs. deleterious responses to oxidative stress in striated muscle

et al. 2014

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“…For instance, sevoflurane has been shown to offer cardioprotection through ROS-mediated upregulation of autophagy in I/R. 8 On the contrary, in vitro evidence suggested that α-lipoic acid protects H9C2 myoblasts against hypoxia/ reoxygenation injury through suppression of autophagy. 9 The precise role of autophagy regulation contributing to cell survival and death in ischemic hearts remains controversial.…”

Section: Induction In I/r Injurymentioning

confidence: 99%

Targeting Autophagy for the Therapeutic Application of Histone Deacetylase Inhibitors in Ischemia/Reperfusion Heart Injury

Zhang

Ren

2014

Circulation

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Editorial 1088I schemic heart disease is a leading cause of morbidity and mortality in the United States and other parts of the world. Despite therapeutic breakthroughs over the past decades such as percutaneous coronary intervention, antiplatelet and antithrombotic therapies, and angioplasty, the prevalence of ischemic heart diseases remains extremely high and constitutes a devastating factor for heart failure.1,2 Among various therapeutic strategies for ischemic heart disease, enormous efforts have been made to limit ischemia/reperfusion (I/R) injury, which occurs when the ischemic myocardium is reperfused with oxygen and substrate-rich blood, which paradoxically worsens heart function.2 Ischemic myocardium, with nutrient and oxygen deprivation and buildup of reactive oxygen species (ROS), uses glycolysis as the primary source of metabolic energy. As a consequence, metabolic acidosis, hyperkalemia, and Ca 2+ overload develop in cardiomyocytes after coronary artery occlusion, leading not only to cardiomyocyte apoptosis during the acute phase but also to delayed adverse myocardial remodeling, which further compromises cardiac function.2 Therefore, limiting I/R-induced myocardial ROS accumulation and apoptosis benefits both short-and long-term survival and quality of life. Although the mechanism responsible for I/R-induced cardiac abnormalities has been focused largely on necrosis and type I (apoptotic) programmed cell death, 2 an intriguing and provocative paradigm has emerged recently that highlights a unique role for dysregulated macroautophagy (hereafter referred to as autophagy) in the heart that may render cardiomyocytes more prone to I/R injury and long-term postinfarction cardiac remodeling.1,3 It has been perceived that autophagy induced by ischemic preconditioning is essential for cardioprotection. To this end, new and innovative strategies to maintain or restore myocardial autophagy homeostasis and its attendant, cardiomyocyte survival, have been the subject of intensive investigation. Article see p 1139The Janus-Faced Role of Autophagy Induction in I/R Injury Autophagy is a tightly regulated, lysosome-dependent catabolic process responsible for turnover of long-lived proteins and intracellular structures that are damaged or malfunctioning. 4,5 The evolutionally conserved bulk degradation process is turned on when cells experience stress, including nutrient and energy deprivation. The autophagic pathway consists of 4 distinct but consecutive steps: initiation, formation of autophagosomes (ie, the double-membrane structures that encircle cargo of damaged cytosolic constituents), generation of autophagolysosomes via docking and fusion with lysosomes, and final degradation of sequestered cargo. Sequestration of cytoplasmic cargo such as long-lived proteins, damaged organelles, and protein aggregates into the double-membrane vesicle autophagosomes occurs before fusion with lysosomes for degradation of its contents by acidic hydrolases. Although physiological levels of autophagy are essential for mitochondr...

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“…Although some studies favor intravenous maintenance of anaesthesia (9,10), in terms of safety and hemodynamic stability, one must remember that new inhaled anaesthetics such as sevoflurane offer both cardioprotection and ease of administration (11,12). A balanced approach (13) using both intravenous and inhaled agents has been proposed and probably offers the potential benefits of both techniques.…”

Section: Discussion Discussionmentioning

confidence: 99%

A New Protocol of Inhalatory Induction of Anaesthesia in Experimental Swine Surgery. A Pilot Study

Popescu¹,

David²,

Pautov³

et al. 2016

JTMR

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Induction of Anaesthesia in swine may prove to be difficult because of the differences in anatomy and physiology. Intubation of large animals is especially difficult due to the length of the snout and the relative difficulty of obtaining adequate relaxation. The present study is aimed to compare two induction techniques for tracheal intubation in pigs. The secondary aim was to assess the effectiveness of a new anaesthetic protocol for experimental surgery. For this, six female pigs underwent two liver surgeries each. Induction of anaesthesia was performed either using intravenous propofol and fentanyl (IV intravenous group) or by using Sevoflurane (inhalatory group). The attending anaesthesiologist was asked to grade the ease of intubation from a scale between 1 and 5. Orotracheal intubation was easier to obtain in the inhalatory group (p=0.00) and a smaller number of attempts were necessary (p=0.00). A lower End-tidal CO2 after intubation was observed in the inhalatory group (p=0.05). There were no differences in both systolic (p=0.11) and diastolic (p=0.72) arterial pressure and heart rate (p=0.16) after induction of anaesthesia between the two groups. Maintenance of anaesthesia was made using Sevoflurane and boluses of fentanyl for adequate analgesia while no muscle relaxants were used. Intravenous morphine and ketoprofen were used for postoperative analgesia. In conclusion, volatile induction of anaesthesia is safe and offers a better view of the larynx in large swine, while the proposed anaesthetic protocol provides adequate anaesthesia for the surgeons and assures comfort to the animals.

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Sevoflurane induces cardioprotection through reactive oxygen species-mediated upregulation of autophagy in isolated guinea pig hearts

Cited by 35 publications

References 32 publications

The â€œGoldilocks Zoneâ€ from a redox perspectiveâ€”Adaptive vs. deleterious responses to oxidative stress in striated muscle

The â€œGoldilocks Zoneâ€ from a redox perspectiveâ€”Adaptive vs. deleterious responses to oxidative stress in striated muscle

Targeting Autophagy for the Therapeutic Application of Histone Deacetylase Inhibitors in Ischemia/Reperfusion Heart Injury

A New Protocol of Inhalatory Induction of Anaesthesia in Experimental Swine Surgery. A Pilot Study

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Sevoflurane induces cardioprotection through reactive oxygen species-mediated upregulation of autophagy in isolated guinea pig hearts

Cited by 35 publications

References 32 publications

The â€œGoldilocks Zoneâ€ from a redox perspectiveâ€”Adaptive vs. deleterious responses to oxidative stress in striated muscle

The â€œGoldilocks Zoneâ€ from a redox perspectiveâ€”Adaptive vs. deleterious responses to oxidative stress in striated muscle

Targeting Autophagy for the Therapeutic Application of Histone Deacetylase Inhibitors in Ischemia/Reperfusion Heart Injury

A New Protocol of Inhalatory Induction of Anaesthesia in Experimental Swine Surgery. A Pilot Study

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Product

Resources

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The â€œGoldilocks Zoneâ€ from a redox perspectiveâ€”Adaptive vs. deleterious responses to oxidative stress in striated muscle

The â€œGoldilocks Zoneâ€ from a redox perspectiveâ€”Adaptive vs. deleterious responses to oxidative stress in striated muscle