Mechanism of Preconditioning by Isoflurane in Rabbits: A Direct Role for Reactive Oxygen Species

Tanaka, Katsuya; Weihrauch, Dorothée; Kehl, Franz; Ludwig, Lynda M.; LaDisa, John F.; Kersten, Judy R.; Pagel, Paul S.; Warltier, David C.

doi:10.1097/00000542-200212000-00021

Cited by 142 publications

(74 citation statements)

References 34 publications

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“…Administration of K ATP channel blocker before isoflurane administration completely blocked the cardioprotection (Tanaka et al, 2003). Isoflurane preconditioning may act via release of small quantities of free radicals to protect myocardium against infarction in rabbits (Mullenheim et al, 2002;Tanaka et al, 2002). Radicals are released from the mitochondria as a consequence of K ATP channel opening (Duranteau et al, 1998;Kowaltowski et al, 2001;McPherson and Yao, 2001a).…”

Section: Discussionmentioning

confidence: 99%

Cardioprotective effects of anesthetic preconditioning in rats with ischemia-reperfusion injury: propofol versus isoflurane

Xing

Lü

et al. 2009

J. Zhejiang Univ. Sci. B

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Abstract:Objective: We compare the cardioprotective effects of anesthetic preconditioning by propofol and/or isoflurane in rats with ischemia-reperfusion injury. Methods: Male adult Wistar rats were subjected to 60 min of anterior descending coronary artery occlusion followed by 120 min of reperfusion. Before the long ischemia, anesthetics were administered twice for 10 min followed by 5 min washout. Isoflurane was inhaled at 1 MAC (0.016) in I group, whereas propofol was inhaled intravenously at 37.5 mg/(kg⋅h) in P group. A combination of isoflurane and propofol was administered simultaneously in I+P group. Results: In control (without anesthetic preconditioning, C group), remarkable myocardial infarction and apoptosis accompanied by an increased level of cardiac troponin T were noted 120 min after ischemia-reperfusion. As compared to those of control group, I and P groups had comparable cardioprotection. In addition, I+P group shares with I and P groups the comparable cardioprotective effects in terms of myocardial infarction and cardiac troponin T elevation. Conclusion: A combination of isoflurane and propofol produced no additional cardioprotection.

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Section: Discussionmentioning

confidence: 99%

Cardioprotective effects of anesthetic preconditioning in rats with ischemia-reperfusion injury: propofol versus isoflurane

Xing

Lü

et al. 2009

J. Zhejiang Univ. Sci. B

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“…In the study by Preckel et al, 15 isoflurane had no effect on infarct size when administered only during the initial perfusion period. However, inhaled isoflurane has been shown to reduce infarct size in the acute memory phase in rats, 16 rabbits, 17 and dogs 18 when discontinued 15-30 min before LAD occlusion. We 4 and others 3 have previously demonstrated that emulsified isoflurane produces cardioprotection.…”

Section: Discussionmentioning

confidence: 99%

The protective effects of emulsified isoflurane on myocardial ischemia and reperfusion injury in rats

Luo

Liu

2008

Can J Anesth/J Can Anesth

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Purpose Pretreatment with volatile anesthetics has been demonstrated to exert cardioprotective effects. The purpose of this study was to examine the effect of emulsified isoflurane, a new formulation of isoflurane in lipid emulsion, administered intravenously in an ischemia and reperfusion model of myocardial injury. Methods Thirty-two Sprague Dawley rats of both sexes were subjected to 30 min of myocardial ischemia followed by 180 min of reperfusion. Each was assigned to one of four pretreatment groups to receive an isovolumetric intravenous infusion of saline: control group, 30% intralipid group, 8% emulsified isoflurane 2 ml kg -1 group, and sham group (each group, n = 8). The vehicles were administered at a constant rate for 30 min and then discontinued 30 min before left anterior descending coronary artery occlusion. The cardioprotective effects were examined by determining hemodynamics, infarct size, enzyme activity, and cardiomyocytic apoptosis. Results Pretreatment with emulsified isoflurane 2 ml kg -1 (P = 0.000) significantly reduced infarct size (22.6 ± 2.2%) compared with control (34.8 ± 2.3%) and 30% intralipid (31.1 ± 2.9%). When compared with the control and intralipid groups, emulsified isoflurane increased Bcl-2 expression while decreasing Bax and Caspase-3 expression and enhancing Bcl-2/Bax ratios. The apoptotic index in the emulsified isoflurane treatment group showed a significant reduction compared with that in the control group (P = 0.000) and the intralipid group (P = 0.001). In addition, the serum levels of lactate dehydrogenase and creatine kinase were markedly reduced in the emulsified isoflurane treatment group compared with the control and intralipid groups (lactate dehydrogenase, P = 0.015 vs. control; creatine kinase, P = 0.000 vs. control and intralipid). Conclusion These data support a cardioprotective effect of intravenous emulsified isoflurane against myocardial ischemia and reperfusion injury, which are mediated, at least in part, by the inhibition of apoptosis and cell damage. RésuméObjectif Il a e´te´de´montre´que les agents anesthe´siques volatils exercent un effet cardioprotecteur lorsqu'ils sont administre´s en traitement pre´ventif. L'objectif de cette e´tude e´tait d'examiner l'effet d'une e´mulsion d'isoflurane, une nouvelle formulation d'isoflurane en e´mulsion lipidique, administre´e par voie intraveineuse dans un mode`le d'ische´mie reperfusion de le´sion myocardique. Méthode Trente-deux rats Sprague Dawley des deux sexes ont e´te´soumis a`30 min d'ische´mie myocardique suivie de 180 min de reperfusion. Chaque rat a e´te´rand-omise´dans l'un des quatre groupes de pre´traitement suivants, recevant tous une perfusion intraveineuse isovolume´trique de solution saline : groupe te´moin, groupe intralipide 30%, groupe e´mulsion d'isoflurane 8% 2 mL kg -1 , et groupe sans intervention (pour chaque groupe, n = 8). Les ve´hicules ont e´te´administre´s à un taux constant durant 30 min puis interrompu 30 min avant l'occlusion de l'arte`re coronaire descendante ante´rieure

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“…One possible mechanism would be their ability to reduce neuronal excitability through enhanced inhibitory and depressed excitatory synaptic transmission (101)(102)(103). It has been reported that small bursts of ROS production may initiate preconditioning in the myocardium (104,105), and that isoflurane induced such a ROS production by inhibiting the respiratory chain in myocardial mitochondria (106). VA may also precondition brain against ischemia by activating mito K ATP (107,108 -uptake (37,110), and thus prevent the activation of necrotic and apoptotic pathways or attenuate the oxidative stress (111).…”

Section: Volatile Anaesthetics and Clinical Implicationsmentioning

confidence: 99%

Sevoflurane depolarizes pre‐synaptic mitochondria in the central nervous system

Moe¹,

Bains²,

Vinje³

et al. 2004

Acta Anaesthesiol Scand

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Background: Volatile anaesthetics protect the heart from ischaemic injury by activating mitochondrial signalling pathways. The aim of this study was to test whether sevoflurane, which is increasingly used in neuroanaesthesia, affects mitochondrial function in the central nervous system by altering the mitochondrial membrane potential (ΔΨm).Methods: In order to correlate free cytosolic Ca2+ ([Ca2+]i) and ΔΨm, rat neural presynaptic terminals (synaptosomes) were loaded with the fluorescent probes fura‐2 and JC‐1. During sevoflurane exposure, 4‐aminopyridine (4‐AP) 500 µM to induce pre‐synaptic membrane depolarization or carbonylcyanide‐p‐(trifluoromethoxy)‐phenylhydrazone (FCCP) 1 µM to induce maximum mitochondrial depolarization was added. In order to block mitochondrial ATP‐regulated K+‐channels (mitoKATP), the antagonist 5‐hydroxydecanoate (5‐HD) 500 µM was added.Results: In Ca2+‐containing medium, both sevoflurane 1 and 2 MAC gradually decreased the normalized JC‐1 ratio from 0.96 ± 0.01 in control to 0.92 ± 0.01 and 0.89 ± 0.01, representing a depolarization of ΔΨm (n = 9, P < 0.05). Sevoflurane 2 MAC increased [Ca2+]i. In Ca2+‐depleted medium, sevoflurane 1 and 2 MAC depolarized ΔΨm, while [Ca2+]i remained unaltered. Sevoflurane 2 MAC attenuated the 4‐AP‐induced depolarization of ΔΨm. When mitoKATP was blocked, the sevoflurane‐induced depolarization of ΔΨm was attenuated, but not blocked. The depolarizing effect of sevoflurane on ΔΨm compared with FCCP was calculated to 13.2 ± 1.3% in Ca2+‐containing and 15.1 ± 1.2% in Ca2+‐depleted medium (n = 7).Conclusions: Sevoflurane depolarizes ΔΨm in rat synaptosomes, and the effect is not dependent on Ca2+‐influx to the cytosol. Opening of mitoKATP is partly responsible for the depolarizing effect of sevoflurane.

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Mechanism of Preconditioning by Isoflurane in Rabbits: A Direct Role for Reactive Oxygen Species

Cited by 142 publications

References 34 publications

Cardioprotective effects of anesthetic preconditioning in rats with ischemia-reperfusion injury: propofol versus isoflurane

Cardioprotective effects of anesthetic preconditioning in rats with ischemia-reperfusion injury: propofol versus isoflurane

The protective effects of emulsified isoflurane on myocardial ischemia and reperfusion injury in rats

Sevoflurane depolarizes pre‐synaptic mitochondria in the central nervous system

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