ArticleJournal of anesthesia2010
Sevoflurane postconditioning prevents activation of caspase 3 and 9 through antiapoptotic signaling after myocardial ischemia-reperfusion.
Article in Journal of anesthesia, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 51 citations in OpenAlex.
- Constitutive activation of ERK1/2 signaling protects against myocardial ischemia via inhibition of mitochondrial fragmentation in the aging heart.Annals of translational medicine · 2021Article
- Effects of Sevoflurane on Apoptosis of Myocardial Cells in IRI Rats.BioMed research international · 2021Article
- Sevoflurane attenuates cardiomyocyte apoptosis by mediating the miR-219a/AIM2/TLR4/MyD88 axis in myocardial ischemia/reperfusion injury in mice.Cell cycle (Georgetown, Tex.) · 2020Article
- Identification and profiling of microRNAs expressed in oral buccal mucosa squamous cell carcinoma of Chinese hamster.Scientific reports · 2019Article
- Effects of sevoflurane pretreatment on the apoptosis of rat H9c2 cardiomyocytes and the expression of GRP78.Experimental and therapeutic medicine · 2018Article
- Cobalt Chloride Upregulates Impaired HIF-1α Expression to Restore Sevoflurane Post-conditioning-Dependent Myocardial Protection in Diabetic Rats.Frontiers in physiology · 2017Article
- Sevoflurane postconditioning improves myocardial mitochondrial respiratory function and reduces myocardial ischemia-reperfusion injury by up-regulating HIF-1.American journal of translational research · 2016Article
- Sevoflurane post-conditioning reduces rat myocardial ischemia reperfusion injury through an increase in NOS and a decrease in phopshorylated NHE1 levels.International journal of molecular medicine · 2015Article
- Sevoflurane Post-conditioning Protects Primary Rat Cortical Neurons Against Oxygen-Glucose Deprivation/Resuscitation: Roles of Extracellular Signal-Regulated Kinase 1/2 and Bid, Bim, Puma.Neurochemical research · 2015Article
- Effect of combination therapy of propofol and sevoflurane on MAP2K3 level and myocardial apoptosis induced by ischemia-reperfusion in rats.International journal of clinical and experimental medicine · 2015Article
- Sevoflurane postconditioning protects rat hearts against ischemia-reperfusion injury via the activation of PI3K/AKT/mTOR signaling.Scientific reports · 2014Article
- Sevoflurane post-conditioning protects isolated rat hearts against ischemia-reperfusion injury via activation of the ERK1/2 pathway.Acta pharmacologica Sinica · 2014Article
- Cellular signaling pathways and molecular mechanisms involving inhalational anesthetics-induced organoprotection.Journal of anesthesia · 2014Review
- Combination of necroptosis and apoptosis inhibition enhances cardioprotection against myocardial ischemia-reperfusion injury.Journal of anesthesia · 2014Article
- Activation of Akt and cardioprotection against reperfusion injury are maximal with only five minutes of sevoflurane postconditioning in isolated rat hearts.Journal of Zhejiang University. Science. B · 2013Article
- Post-conditioning: promising answers and more questions.Critical care (London, England) · 2012Article
- The effect of sevoflurane postconditioning on cardioprotection against ischemia-reperfusion injury in rabbits.Molecular biology reports · 2012Article
- Pharmacological postconditioning with sevoflurane after cardiopulmonary resuscitation reduces myocardial dysfunction.Critical care (London, England) · 2011Article
- Sevoflurane postconditioning reduces myocardial reperfusion injury in rat isolated hearts via activation of PI3K/Akt signaling and modulation of Bcl-2 family proteins.Journal of Zhejiang University. Science. B · 2010Article
- [The effect of anesthetic preconditioning with sevoflurane on intracellular signal-transduction pathways and apoptosis, in a lung autotransplant experimental model].Brazilian journal of anesthesiology (Elsevier)Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeVolatile anesthetic postconditioning reduces apoptosis through antiapoptotic signaling. Whether sevoflurane postconditioning prevents activation of caspase 9 and 3, which are implicated in the initiation and execution step of apoptosis, is not known.
methodsIsolated perfused guinea pig hearts underwent 30 min global ischemia and 120 min reperfusion [control (CTL)]. Anesthetic postconditioning was elicited with sevoflurane (2%) for 2 min at reperfusion onset (POST). LY294002, phosphatidylinositol-3-kinase (PI3K)/Akt (protein kinase B) inhibitor; and PD98059, extracellular signal-regulated kinase 1/2 (ERK) inhibitor, were administered for 10 min before ischemia and throughout the reperfusion period in POST (POST + LY, POST + PD). Left-ventricular-developed (LVDP) and LV end-diastolic (LVEDP) pressures and infarct size were measured. Western blot analysis determined phosphorylated Akt and ERK expression. Myocardial caspase 3 and 9 were determined immunohistochemically.
resultsAfter ischemia-reperfusion, POST had higher LVDP (57 +/- 9 vs. 38 +/- 7 mmHg, p < 0.05) and lower LVEDP (21 +/- 8 vs. 46 +/- 15 mmHg, p < 0.05) versus CTL. Infarct size was significantly reduced in POST versus CTL (15 +/- 3 vs. 41 +/- 11%, p < 0.001). Phosphorylation of Akt and ERK after reperfusion was significantly increased in POST versus CTL. Immunoreactivity for caspase 3 and 9 was greater in the nucleus of myocytes and endothelial cells in CTL. POST attenuated this increased immunoreactivity. LY294002 and PD98059 abolished the effect of POST on caspase 3 and 9 immunoreactivity.
conclusionsSevoflurane postconditioning prevents activation of caspase 3 and 9, mediators of apoptosis in ischemia-reperfusion injury. This caspase activation is mediated by phosphorylation of Akt and ERK.
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