Comparative effects of halothane, enflurane, isoflurane and sevoflurane on function and metabolism in the ischaemic rat heart

Oguchi, Takeshi; Kashimoto, Satoshi; Yamaguchi, Tasuku; Nakamura, Toshihiro; Kumazawa, Teruo

doi:10.1093/bja/74.5.569

Cited by 50 publications

(25 citation statements)

References 26 publications

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“…14 Sevoflurane does not influence intracellular 5Ј-AMP levels in the heart, and no effects of sevoflurane were found on intracellular myocardial ATP levels. 15 Thus, alternative mechanisms of AMPK activation should be considered.…”

Section: Discussionmentioning

confidence: 99%

Reactive Oxygen Species–Induced Stimulation of 5′AMP-Activated Protein Kinase Mediates Sevoflurane-Induced Cardioprotection

et al. 2009

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Background-5ЈAMP-activated protein kinase (AMPK), a well-known regulator of cellular energy status, is also implicated in ischemic preconditioning leading to cardioprotection. We hypothesized that AMPK is involved in anesthetic-induced cardioprotection and that this activation is mediated by reactive oxygen species (ROS). Methods and Results-Isolated Langendorff-perfused rat hearts were subjected to 35 minutes of global ischemia (I) followed by 120 minutes of reperfusion (I/R). Hearts were assigned to a control group (Con) or a sevoflurane (Sevo) group receiving 3 times 5-minute episodes of sevoflurane (2.5vol%) before I/R. Phosphorylation of both AMPK and endothelial nitric oxide synthase (eNOS) were determined by Western blot analysis. Cardioprotection was assessed after I/R from recovery of left ventricular pressure and from infarct size (triphenyltetrazolium chloride staining). In the control group, ischemia resulted in a 2-fold increase in phosphorylation levels of AMPK (Con 0.13Ϯ0.01 versus Con-I 0.28Ϯ0.05, PϽ0.05), which was sustained after 120 minutes of reperfusion (Con-I/R 0.26Ϯ0.02, PϽ0.05). Sevoflurane preconditioning had no affect on AMPK phosphorylation before ischemia (Sevo 0.12Ϯ0.03, PϾ0.05), but almost doubled the increase in AMPK phosphorylation relative to control after ischemia (Sevo-I 0.48Ϯ0.09, PϽ0.05), an effect that was sustained after reperfusion (Sevo-I/R 0.49Ϯ0.12, PϽ0.05). The AMPK-inhibitor compound C (10 mol/L) reduced the sevoflurane-mediated increase in phosphorylation of AMPK and its target eNOS and abolished cardioprotection. The ROS-scavenger n-(2-mercaptopropionyl)-glycine (1 mmol/L) blunted the sevoflurane-mediated increase in AMPK and eNOS phosphorylation and prevented cardioprotection. Conclusions-Sevoflurane-induced AMPK activation protects the heart against ischemia and reperfusion injury and relies on upstream production of ROS. (Circulation. 2009;120[suppl 1]:S10-S15.)

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Section: Discussionmentioning

confidence: 99%

Reactive Oxygen Species–Induced Stimulation of 5′AMP-Activated Protein Kinase Mediates Sevoflurane-Induced Cardioprotection

et al. 2009

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“…Although a portion of the acute cardioprotective effects of volatile anesthetics following ischemia and reperfusion may be attributed to a reduction in energy requirements and ultimate preservation of energy-dependent vital cellular processes, other studies have demonstrated this not to be necessary for cardioprotection. For example, halothane exerts cardioprotective effects even when administered during cardioplegic arrest and at reperfusion (31,38). Thus a decrease in oxygen demand is unlikely to be the only mechanism responsible for the acute anti-ischemic actions of volatile anesthetics.…”

Section: Discussionmentioning

confidence: 99%

Delayed cardioprotection by isoflurane: role of K_ATP channels

Tonkovic-Capin¹,

Gross²,

Bošnjak³

et al. 2002

American Journal of Physiology-Heart and Circulatory Physiology

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Isoflurane mimics the cardioprotective effect of acute ischemic preconditioning with an acute memory phase. We determined whether isoflurane can induce delayed cardioprotection, the involvement of ATP-sensitive potassium (KATP) channels, and cellular location of the channels. Neonatal New Zealand White rabbits at 7-10 days of age (n ϭ 5-16/group) were exposed to 1% isoflurane-100% oxygen for 2 h. Hearts exposed 2 h to 100% oxygen served as untreated controls. Twenty-four hours later resistance to myocardial ischemia was determined using an isolated perfused heart model. Isoflurane significantly reduced infarct size/area at risk (means Ϯ SD) by 50% (10 Ϯ 5%) versus untreated controls (20 Ϯ 6%). Isoflurane increased recovery of preischemic left ventricular developed pressure by 28% (69 Ϯ 4%) versus untreated controls (54 Ϯ 6%). The mitochondrial KATP channel blocker 5-hydroxydecanoate (5-HD) completely (55 Ϯ 3%) and the sarcolemmal KATP channel blocker HMR 1098 partially (62 Ϯ 3%) attenuated the cardioprotective effects of isoflurane. The combination of 5-HD and HMR-1098 completely abolished the cardioprotective effect of isoflurane (56 Ϯ 5%). We conclude that both mitochondrial and sarcolemmal KATP channels contribute to isoflurane-induced delayed cardioprotection. ischemia; heart; infarct size; volatile anesthetics; myocardial preconditioning BRIEF PERIODS OF ISCHEMIA lead to a reduced severity of cardiac injury following a second sustained period of ischemia. This cardioprotective effect has been termed ischemic preconditioning and has been demonstrated in all species studied. Certain pharmacological agents can mimic the cardioprotective effect of ischemic preconditioning. Recent clinical and experimental data indicate that volatile anesthetics also exert acute protective effects on the myocardium.The protective effects of volatile anesthetics on ischemic myocardium have been termed anesthetic-induced preconditioning because of its remarkable similarity to ischemic preconditioning. Isoflurane improves functional recovery of stunned myocardium in chronically or acutely instrumented dogs after brief periods of coronary artery occlusion and reperfusion (25,26,44). Low doses of the ATP-sensitive K (K ATP ) channel blocker glibenclamide completely abolished the cardioprotective effects of isoflurane (25). These results indicate that K ATP channels are activated by isoflurane and mediate the beneficial effects of isoflurane in stunned myocardium in animal models that respond to acute ischemic preconditioning in a similar fashion to the human heart (5, 45).K ATP channel openers mimic early ischemic preconditioning, whereas K ATP channel blockers prevent ischemic preconditioning. These effects were initially attributed to opening and closing of sarcolemmal K ATP channels, respectively. New evidence suggests, however, that mitochondrial K ATP channels might very well have even a greater influence on preconditioning (35, 37). For instance, diazoxide, an opener of mitochondrial K ATP channels, was demonstrated to exert ca...

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“…A possible mechanism of this protective effect includes stimulation of the adenosine receptor and K ATP channel [32,33], suppression of metabolism [34], reduction of the frequency of transient ischemic depolarizations [35], and activation of protein kinase C [36]. Recently, reduction of leukocyte adhesion has also been proposed for the protection mechanism [8,37].…”

Section: Discussionmentioning

confidence: 99%

Inhibition of E-selectin-mediated leukocyte adhesion by volatile anesthetics in a static condition

et al. 2005

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Comparative effects of halothane, enflurane, isoflurane and sevoflurane on function and metabolism in the ischaemic rat heart

Cited by 50 publications

References 26 publications

Reactive Oxygen Species–Induced Stimulation of 5′AMP-Activated Protein Kinase Mediates Sevoflurane-Induced Cardioprotection

Reactive Oxygen Species–Induced Stimulation of 5′AMP-Activated Protein Kinase Mediates Sevoflurane-Induced Cardioprotection

Delayed cardioprotection by isoflurane: role of K_ATP channels

Inhibition of E-selectin-mediated leukocyte adhesion by volatile anesthetics in a static condition

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Comparative effects of halothane, enflurane, isoflurane and sevoflurane on function and metabolism in the ischaemic rat heart

Cited by 50 publications

References 26 publications

Reactive Oxygen Species–Induced Stimulation of 5′AMP-Activated Protein Kinase Mediates Sevoflurane-Induced Cardioprotection

Reactive Oxygen Species–Induced Stimulation of 5′AMP-Activated Protein Kinase Mediates Sevoflurane-Induced Cardioprotection

Delayed cardioprotection by isoflurane: role of KATP channels

Inhibition of E-selectin-mediated leukocyte adhesion by volatile anesthetics in a static condition

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Delayed cardioprotection by isoflurane: role of K_ATP channels