sevoflurane postconditioning

BACKGROUND: Sevoflurane (Sevo) preconditioning and postconditioning play a protective role against injury induced by hepatic ischemia/reperfusion (I/R). At the same time, the involvement of macrophage infiltration in this process and the precise mechanisms are unclear. Here, we designed this research to elucidate the protective effects of Sevo against hepatic I/R injury and the molecules involved. METHODS: The alleviating effect of Sevo on the liver injury was analyzed by liver function analysis, hematoxylin and eosin staining, Masson trichrome staining, terminal deoxynucleotidyl transferase-mediated 2'-deoxyuridine 5'-triphosphate nick end labeling, western blot analysis and an enzyme-linked immunosorbent assay...

Sevoflurane postconditioning has been shown to provide neuroprotection against cerebral hypoxia-ischemia injury, but the mechanisms remain elusive. Microtubule-associated protein 2 (MAP2) is implicated in early neuronal hypoxia-ischemia injury. This study aimed to investigate whether the neuroprotective effects of sevoflurane postconditioning are related to the Akt/GSK-3β pathway and its downstream target MAP2 in zebrafish hypoxia/reoxygenation (H/R) model. Sevoflurane postconditioning or GSK-3β inhibitor TDZD-8 were used to treat H/R zebrafish...

BACKGROUND: Subarachnoid hemorrhage (SAH) is associated with neurocognitive impairment. Recent data suggest that sevoflurane attenuates edema formation after SAH in rats. However, so far, no information is available about the long-term repair phase, nor if sevoflurane impacts functionality by increasing vascularity. This study tested whether sevoflurane postconditioning would improve long-term neurologic deficit through increased formation of new vessels close to the hemorrhage area. METHODS: Fifty-three animals were subjected to SAH or sham surgery with or without a 2-hour sevoflurane postconditioning (versus propofol anesthesia)...

Hypoxic-ischemic brain damage (HIBD) frequently induces cognitive impairments. Investigating the role of sevoflurane postconditioning (SPC) in HIBD, we conducted experiments involving HIBD modeling, SPC treatment, and interventions with the PERK inhibitor GSK2656157 or the PERK activator CCT020312, administered 30 min before modeling, followed by SPC treatment. Behavioral testing using the Morris water maze test and Neurological Deficiency Scale (NDS) was conducted. Additionally, Nissl staining assessed hippocampal CA1 area neuronal density, TUNEL staining evaluated hippocampal CA1 area neuronal apoptosis, and Western blot determined hippocampal CA1 area protein levels, including Bax, Bcl-2, p-PERK/PERK, p-eIF2/eIF2, ATF4, CHOP, GRP78, Bax, and Bcl-2 protein levels...

In the last few years, the use of anesthetic drugs has been related to effects other than those initially related to their fundamental effect, hypnosis. Halogenated anesthetics, mainly sevoflurane, have been used as a therapeutic tool in patients undergoing cardiac surgery, thanks to the beneficial effect of the cardiac protection they generate. This effect has been described in several research studies. The mechanism by which they produce this effect has been associated with the effects generated by anesthetic preconditioning and postconditioning...

Myocardial infarction (MI) has been considered a leading cause of death worldwide. Relieving ischemia-reperfusion myocardial damage is one of the major roles in treating MI. Sevoflurane postconditioning provides myocardial protection, and this study probes the mechanism of sevoflurane-mediated protective effects. A hypoxia/reoxygenation (H/R) model was constructed in cardiomyocytes, which were pretreated with 2.4% sevoflurane. Alterations in SNHG10, miR-495-3p, and PTEN levels were determined, and gain- or loss-of functional assays were conducted to confirm the role of the SNHG10/miR-495-3p axis, which is potentially regulated by sevoflurane...

BACKGROUND: The volatile anaesthetic sevoflurane protects cardiac tissue from reoxygenation/reperfusion. Mitochondria play an essential role in conditioning. We aimed to investigate how sevoflurane and its primary metabolite hexafluoroisopropanol (HFIP) affect necrosis, apoptosis, and reactive oxygen species formation in cardiomyocytes upon hypoxia/reoxygenation injury. Moreover, we aimed to describe the similarities in the mode of action in a mitochondrial bioenergetics analysis. METHODS: Murine cardiomyocytes were exposed to hypoxia (0...

OBJECTIVE: The ProCCard study tested whether combining several cardioprotective interventions would reduce the myocardial and other biological and clinical damage in patients undergoing cardiac surgery. DESIGN: Prospective, randomized, controlled trial. SETTING: Multicenter tertiary care hospitals. PARTICIPANTS: 210 patients scheduled to undergo aortic valve surgery. INTERVENTIONS: A control group (standard of care) was compared to a treated group combining five perioperative cardioprotective techniques: anesthesia with sevoflurane, remote ischemic preconditioning, close intraoperative blood glucose control, moderate respiratory acidosis (pH 7...

Sevoflurane is the most commonly used anesthetic in clinical practice and exerts a protective effect on cerebral ischemia-reperfusion (I/R) injury. This study aims to elucidate the molecular mechanism by which sevoflurane postconditioning protects against cerebral I/R injury. Oxygen-glucose deprivation/reperfusion (OGD/R) model in vitro and the middle cerebral artery occlusion (MCAO) model in vivo were established to simulate cerebral I/R injury. Sevoflurane postconditioning reduced neurological deficits, cerebral infarction, and ferroptosis after I/R injury...

Ischemia-reperfusion injury (IRI) is an inflammatory process inherent in organ transplantation procedures. It is associated with tissue damage and, depending on its intensity, can impact early graft function. In liver transplantation (LT), strategies to alleviate IRI are essential in order to increase the use of extended criteria donor (ECD) grafts, which are more susceptible to IRI, as well as to improve postoperative graft and patient outcomes. Sevoflurane, a commonly used volatile anesthetic, has been shown to reduce IRI...

To determine whether sevoflurane postconditioning protects against cerebral ischemia reperfusion (I/R) injury and its potential mechanism, we employed bioinformatic analysis, neurological assessments, and western blot analysis, as well as triphenyl tetrazolium chloride, hematoxylin and eosin, Nissl, and immunofluorescence staining. We identified 103 differentially expressed genes induced by cerebral I/R, including 75 upregulated genes and 28 downregulated genes enriched for certain biological processes (involving regulation of inflammatory responses, cellular responses to interleukin 1, and chemokine activity) and signaling pathways (such as transcriptional misregulation in cancer, interleukin-17 signaling, rheumatoid arthritis, MAPK signaling, and Toll-like receptor signaling)...

AIMS: The study aimed to investigate the protective effects and regulatory mechanism of sevoflurane postconditioning (SPC) in pulmonary apoptosis induced by cardiopulmonary bypass (CPB). METHODS: Twenty-four healthy dogs were divided into a control (C group), ischemia/reperfusion (I/R group), sevoflurane postconditioning (S group), and wortmannin group (S+W group). At 10 min after the establishment of CPB, the left pulmonary artery was blocked. When the pulmonary artery was reopened, 2% sevoflurane was administered...

Objective: Myocardial ischemia/reperfusion injury (IRI) is a common and serious complication in clinical practice. Sevoflurane conditionings have been identified to provide a protection against myocardial IRI in animal experiments, but their true clinical benefits remain controversial. Here, we aimed to analyze the preclinical evidences obtained in animal models of myocardial IRI and explore the possible reasons for controversial clinical benefits. Methods: Our primary outcome was the difference in mean infarct size between the sevoflurane and control groups in animal models of myocardial IRI...

Cerebral ischemia reperfusion injury (IRI) induced by hemorrhagic shock and reperfusion (HSR) is the main cause of death following trauma. Previous studies indicated the neuroprotective effect of sevoflurane postconditioning (SP) in cerebral IRI. However, the mechanisms still remain elusive. Cerebral IRI models with SP were established by using HSR with C57BL/6 mice (male, 3-month-old) in vivo and by using oxygen glucose deprivation and reoxygenation (OGD/R) with HT22 cells in vitro . Postoperative cognition was evaluated by the Morris water maze, novel object recognition, and elevated plus maze tests...

PURPOSE: Extensive reports have demonstrated the neuroprotection of sevoflurane postconditioning under the background of focal and global cerebral ischemia/reperfusion, the underlying mechanisms are not completely elucidated. This study was to investigate if this effect is related to eNOS and mediated by phosphoinositide-3-kinase pathway in a rat model of hemorrhagic shock and resuscitation. METHODS: Adult male Sprague-Dawley rats were subjected to hemorrhagic shock for 60min and then resuscitation for 30min in exprimental groups...

OBJECTIVES: Myocardial ischemia-reperfusion injury is a phenomenon that promotes myocardial damage when the blood supply returns to the tissue after a period of ischemia. Anesthetic postconditioning involves myocardial protection against myocardial I/R injury. The effects of atorvastatin (ATV) on sevoflurane postconditioning against myocardial ischemia-reperfusion injury have not been thoroughly studied. The present study aimed to investigate if ATV interacts synergistically with sevoflurane postconditioning against myocardial infarction in rabbit hearts in vivo...

Sevoflurane postconditioning (SPostC) has been proved effective in cardioprotection against myocardial ischemia/reperfusion injury. It was also reported that heat shock protein 70 (HSP70) could be induced by sevoflurane, which played a crucial role in hypoxic/reoxygenation (HR) injury of cardiomyocytes. However, the mechanism by which sevoflurane protects cardiomyocytes via HSP70 is still not understood. Here, we aimed to investigate the related mechanisms of SPostC inducing HSP70 expression to reduce the HR injury of cardiomyocytes...

Sevoflurane postconditioning (SPC) has been widely reported to attenuate brain injury after hypoxia-ischemia encephalopathy (HIE) by inhibiting neural necrosis and autophagy. Moreover, recent reports revealed that sevoflurane facilitated hippocampal reconstruction via regulating migration. Yet, it remains unclear whether the promotion of neural migration by SPC repairs the hippocampal injury after HIE. Here, we hypothesize that SPC exerts a neuroprotective effect by ameliorating neuronal migration disorder after HIE and regulating Reelin expression...

The cardioprotective effect of sevoflurane postconditioning (SPostC) is lost in diabetes that is associated with cardiac phosphatase and tensin homologue on chromosome 10 (PTEN) activation and phosphoinositide 3-kinase (PI3K)/Akt inactivation. T-LAK cell-originated protein kinase (TOPK), a mitogen-activated protein kinase- (MAPKK-) like serine/threonine kinase, has been shown to inactivate PTEN (phosphorylated status), which in turn activates the PI3K/Akt signaling (phosphorylated status). However, the functions of TOPK and molecular mechanism underlying SPostC cardioprotection in nondiabetes but not in diabetes remain unknown...

Neuroinflammation can cause cognitive deficits, and preexisting neuroinflammation is observed frequently in the clinic after trauma, surgery, and infection. Patients with preexisting neuroinflammation often need further medical treatment under general anesthesia. However, the effects of postconditioning with general anesthetics on preexisting neuroinflammation have not been determined. In this study, adult rats were posttreated with sevoflurane or propofol after intracerebroventricular administration of lipopolysaccharide...