sevoflurane postconditioning

Diabetic hearts are vulnerable to myocardial ischemia/reperfusion injury (IRI), but are insensitive to sevoflurane postconditioning (SPC), activating peroxiredoxins that confer cardioprotection. Previous studies have demonstrated that hydrogen sulfide (H2 S) can suppress oxidative stress of diabetic rats through increasing the expression of silent information regulator factor 2-related enzyme 1 (SIRT1), but whether cardioprotection by SPC can be restored afterward remains unclear. Diabetic rat was subjected to IRI (30 min of ischemia followed by 120 min reperfusion)...

Previous studies have demonstrated that sevoflurane postconditioning can provide neuroprotection after hypoxic-ischemic injury and improve learning and memory function in developing rodent brains. The classical Rice-Vannucci model was used to induce hypoxic-ischemic injury, and newborn (postnatal day 7) rats were treated with 2.4% sevoflurane for 30 minutes after hypoxic-ischemic injury. Our results showed that sevoflurane postconditioning significantly improved the learning and memory function of rats, decreased astrogliosis and glial scar formation, increased numbers of dendritic spines, and protected the histomorphology of the hippocampus...

Inhalation anesthetics have been demonstrated to have protective effects against myocardial ischemia reperfusion injury (MIRI). O-linked GlcNAcylation (O-GlcNAc) modifications have been shown to protect against MIRI. This study aimed to investigate whether O-GlcNAcylation and necroptosis signaling were important for sevoflurane postconditioning (SPC) induced cardioprotective effects. Apart from rats in the SHAM and sevoflurane (SEVO) group, rats underwent 30 min ischemia followed by 2 h reperfusion. Cardiac hemodynamics and function were determined...

Background: Sevoflurane is commonly used as a general anesthetic in neonates to aged patients. Preconditioning or postconditioning with sevoflurane protects neurons from excitotoxic injury. Conversely, sevoflurane exposure induces neurotoxicity during early or late life. However, little is known about the underlying mechanism of the dual effect of sevoflurane on neurons. Autophagy is believed to control neuronal homeostasis. We hypothesized that autophagy determined the dual effect of sevoflurane on neurons...

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BACKGROUND Sevoflurane as a widely used inhalational general anesthetic that also has a cardioprotective role in hypoxia-reoxygenation (H/R) injury. This study aimed to investigate the effects of microRNA-107 (miR-107) on sevoflurane postconditioning (SpostC) in H9C2 embryonic rat cardiomyocytes and to use bioinformatics analysis to identify the molecular basis of cardioprotection from sevoflurane in human cardiac tissue. MATERIAL AND METHODS The STRADA gene was identified from the Gene Expression Omnibus (GEO) database...

Mitochondrial autophagy is involved in myocardial protection of sevoflurane postconditioning (SPostC) and in diabetic state this protective effect is weakened due to impaired HIF-1 signaling pathway. Previous studies have proved that deferoxamine (DFO) could activate impaired HIF-1α in diabetic state to restore the cardioprotective of sevoflurane, while the specific mechanism is unclear. This study aims to investigate whether HIF-1/BNIP3-mediated mitochondrial autophagy is involved in the restoration of sevoflurane postconditioning cardioprotection in diabetic state...

BACKGROUND: Hemorrhagic shock induces the cognitive deficiency. Sevoflurane postconditioning has been documented to provide neuroprotection against ischemic-reperfusion injury by suppressing apoptosis. Mitochondrial permeability transition pore (mPTP) plays an important role in apoptosis, but it is unknown if the protective effect of sevoflurane postconditioning on hemorrhagic shock and resuscitation is associated with the change of mPTP opening. Hence, the aim of the study was to find out the precise mechanism of the sevoflurane postconditioning...

OBJECTIVE: Various experimental studies reported neuroprotective effects of sevoflurane postconditioning against cerebral ischemia-reperfusion injury. We thus investigated its neuroprotective effects on hyperperfusion-related transient neurologic deterioration, called symptomatic cerebral hyperperfusion (SCH) and also identified predictive factors for SCH in moyamoya patients after revascularization surgery. METHODS: 152 adult moyamoya patients undergoing anastomosis of superficial temporal artery to middle cerebral artery were randomly allocated into two groups...

BACKGROUND: Myocardial damage in patients undergoing cardiac surgery increases both morbidity and mortality. Different protective strategies dealing with either preconditioning or postconditioning or assessing a single aspect of cardioprotection have shown conflicting results. We tested the hypothesis that a multimodal approach would improve cardioprotection and limit myocardial damage following cardiac surgery with cardiopulmonary bypass. METHODS: This study is a pragmatic multicenter (six French institutions), prospective, randomized, single-blinded, controlled trial...

BACKGROUND: Preventing myocardial ischemia-reperfusion injury in on-pump cardiac surgeries remains an enormous challenge. Sevoflurane postconditioning has been effective at overcoming this challenge by modulating inflammatory mediators and ameliorating antioxidative stress. Dexmedetomidine (DEX) is a commonly used medication for cardiac patients with organ-protective properties that lead to positive outcomes. Whether DEX also has cardiac-protective properties and the associated mechanism in sevoflurane postconditioning-based valve replacement surgeries are unknown...

Background: Sevoflurane postconditioning (SpostC) can alleviate hypoxia-reoxygenation injury of cardiomyocytes; however, the specific mechanism remains unclear. This study aimed to investigate whether SpostC promotes mitochondrial autophagy through the hypoxia-inducible factor-1 (HIF-1)/BCL2/adenovirus E1B 19-kDa-interacting protein 3 (BNIP3) signaling pathway to attenuate hypoxia-reoxygenation injury in cardiomyocytes. Methods: The H9C2 cardiomyocyte hypoxia/reoxygenation model was established and treated with 2...

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Objective: The inhalation anesthetic sevoflurane has presented numerous biological activities, including anti-inflammatory properties and protective effects against tissue ischemic injury. This study investigated the metabolic, hemodynamic, and inflammatory effects of sevoflurane pre- and postconditioning for short periods in the rescue of liver ischemia-reperfusion (IR) injury using a rat model. Materials and Methods: Twenty Wistar rats were divided into four groups: sham group, control ischemia group (partial warm liver ischemia for 45 min followed by 4 h of reperfusion), SPC group (administration of sevoflurane 2...

This study aimed to investigate the effect of miR-206 on apoptosis and autophagy of cardiomyocytes in ischemia/reperfusion (I/R) injured rats treated with sevoflurane postconditioning (SP) through the AMPK/Nampt signaling pathway. Rat models of myocardial I/R injury were established. The combination of SP, miR-206 inhibitor, AMPK activator AICAR and inhibitor Compound C was induced in rats, and their effects on I/R injury were determined with detection of malondialdehyde (MDA), hydroxyproline (HYP) and superoxide dismutase (SOD) levels in cardiomyocytes, autophagy, and apoptosis...

PURPOSE: Ischemia-reperfusion (IR) injury is inevitable after liver transplantation and liver resection with inflow occlusion. Sevoflurane has been widely used during hepatobiliary surgery and was reported to exhibit preconditioning (PreC) properties against hepatic IR injury; however, its postconditioning (PostC) properties remain unknown. This study examined whether a clinically applicable dose of sevoflurane has PostC and PreC properties against hepatic IR injury and roles of heme oxygenase-1 (HO-1)...

This study aims to investigate the role of microRNA-145 (miR-145) in protection against myocardial ischemia/reperfusion (I/R) injury in mice by regulating expression of granzyme K (GZMK) with the treatment of sevoflurane. The mice model of myocardial I/R injury was established by left coronary artery ligation. The expression of miR-145 and GZMK in myocardial tissues of mice was detected by Reverse transcription quantitative polymerase chain reaction and western blot analysis. The changes of the cardiac function and hemodynamics, pathological changes of myocardial tissues, the ultrastructure of cardiomyocytes, myocardial infarction area, and cardiomyocyte apoptosis were observed...

Application of the commonly used volatile anesthetic sevoflurane after brain ischemia (sevoflurane postconditioning) attenuates ischemic brain injury. It is not known whether autophagy plays a role in this sevoflurane postconditioning-induced neuroprotection. Human SH-SY5Y cells were induced to become neuron-like cells. These cells were subjected to 1h oxygen-glucose deprivation (OGD) and then exposed to sevoflurane for 1h. Chloroquine, an inhibitor of autolysosomes, rapamycin, an autophagy inducer, or 3-methyladenine (3-MA), an autophagy inhibitor, were incubated with cells during OGD and sevoflurane exposure...

BACKGROUND: The neuroprotection and neurotoxicity induced by sevoflurane have been gradually established. Choosing anesthetic agents after hemorrhage shock and resuscitation (HSR) induced by bleeding can be challenging. We determined the dual neuroprotective-neurotoxic effects of sevoflurane postconditioning after HSR injury using a model of blood loss and reinfusion in rats via the heme oxygenase-1 (HO-1)/reactive oxygen species (ROS) signal pathway. METHODS: The rats were exposed to 2%-4% sevoflurane postconditioning in vivo after HSR...