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apoptosis sevo

Hong Xie, Jing Zhang, Jiang Zhu, Li-xin Liu, Mario Rebecchi, Su-mei Hu, Chen Wang
AIM: To investigate the role of extracellular signal-regulated kinases (ERKs) in sevoflurane post-conditioning induced cardioprotection in vitro. METHODS: Isolated rat hearts were subjected to 30 min ischemia followed by 120 min reperfusion (I/R). Sevoflurane post-conditioning was carried out by administration of O2-enriched gas mixture with 3% sevoflurane (SEVO) for 15 min from the onset of reperfusion. Cardiac functions, myocardial infarct size, myocardial ATP and NAD(+) contents, mitochondrial ultrastructure, and anti-apototic and anti-oncosis protein levels were measured...
December 2014: Acta Pharmacologica Sinica
Lionel Pellegrini, Youssef Bennis, Lionel Velly, Isabelle Grandvuillemin, Pascale Pisano, Nicolas Bruder, Benjamin Guillet
INTRODUCTION: Recent data on newborn animals exposed to anesthetics have raised safety concerns regarding anesthesia practices in young children. Indeed, studies on rodents have demonstrated a widespread increase in brain apoptosis shortly after exposure to sevoflurane, followed by long-term neurologic impairment. In this context, we aimed to evaluate the protective effect of rh-EPO, a potent neuroprotective agent, in rat pups exposed to sevoflurane. MATERIAL AND METHODS: At postnatal day 7, 75 rat pups were allocated into three groups: SEVO + EPO (n = 27) exposed to sevoflurane 2 vol% (0...
July 2014: Paediatric Anaesthesia
Hong Xie, Xia Liu, Chen Wang, Jiang Zhu, Chen Yang, Chunfeng Liu, Hong Liu, Xuemei Wu
This study was designed to use real-time imaging to test the hypothesis that delayed cardiac protection induced by volatile anesthetics inhibits apoptosis. Rats were divided into two groups. One group was exposed to 120 min of 33 % O2 [control group (CON group)] and the other group was exposed to 2.5 % sevoflurane in 33 % O2 for 120 min [sevoflurane group (SEVO group)]. Both groups were allowed to return to their cages for 24 h. After 24 h recovery, all rats underwent 30 min myocardial ischemia by occluding coronary artery followed by 2 h of reperfusion...
January 2014: Molecular Biology Reports
S Q Zheng, L X An, X Cheng, Y J Wang
BACKGROUND: Neonatal exposure to sevoflurane can induce neurodegeneration and learning deficits in developing brain. We hypothesised that with the increase in the concentration and duration of sevoflurane, neurodegeneration of neonatal rats aggravates and causes behaviour changes as the rats grow. METHODS: Twenty-one post-natal day (P)7 Wistar rats were randomly divided into seven groups. Blood analysis was performed after anaesthesia. According to the results, 120 P7 Wistar rats were randomly divided into five groups: Con sham anaesthesia; Sevo 1%-2 h: exposed to 1% sevoflurane for 2 h; Sevo 1%-4 h, Sevo 2%-2 h and Sevo 2%-4 h...
October 2013: Acta Anaesthesiologica Scandinavica
Katherine R Gentry, Louise M Steele, Margaret M Sedensky, Philip G Morgan
BACKGROUND: Mounting evidence from animal studies shows that anesthetic exposure in early life leads to apoptosis in the developing nervous system. This loss of neurons has functional consequences in adulthood. Clinical retrospective reviews have suggested that multiple anesthetic exposures in early childhood are associated with learning disabilities later in life as well. Despite much concern about this phenomenon, little is known about the mechanism by which anesthetics initiate neuronal cell death...
January 2013: Anesthesia and Analgesia
Xue Zhou, Fa-Huan Song, Wen He, Xiao-Yu Yang, Zhi-Bin Zhou, Xia Feng, Li-Hua Zhou
A growing number of studies have shown that commonly used anesthetic agents may cause neurohistopathological changes and persistent behavioral impairments in the developing brain. The effects of sevoflurane, a widely used substance in pediatric anesthesia, on the developing brain have not been thoroughly analyzed thus far. In this study, Sprague-Dawley rats at postnatal day (P)7 were exposed to 2.3% sevoflurane for 6 h continuously. Six hours after exposure, hematoxylin and eosin (H&E) staining was used to determine the morphological changes in the hippocampus...
September 2012: Molecular Medicine Reports
Patrick Meybohm, Matthias Gruenewald, Martin Albrecht, Christina Müller, Karina Zitta, Nikola Foesel, Moritz Maracke, Sabine Tacke, Jürgen Schrezenmeir, Jens Scholz, Berthold Bein
INTRODUCTION: In this study, we sought to examine whether pharmacological postconditioning with sevoflurane (SEVO) is neuro- and cardioprotective in a pig model of cardiopulmonary resuscitation. METHODS: Twenty-two pigs were subjected to cardiac arrest. After 8 minutes of ventricular fibrillation and 2 minutes of basic life support, advanced cardiac life support was started. After successful return of spontaneous circulation (N = 16), animals were randomized to either (1) propofol (CONTROL) anesthesia or (2) SEVO anesthesia for 4 hours...
2011: Critical Care: the Official Journal of the Critical Care Forum
Benjamin Drenger, Israel A Ostrovsky, Michal Barak, Yael Nechemia-Arbely, Ehud Ziv, Jonathan H Axelrod
BACKGROUND: The possibility of restoring sevoflurane postconditioning (sevo-postC) cardioprotection in diabetic animals is uncertain. We hypothesized that attenuation of myocardial injury by sevo-postC might be hindered by inhibition of signal transducer and activator of transcription (STAT) 3-regulated activity of phosphatidylinositol 3-kinase (PI3K) in diabetic animals. To determine whether postC cardioprotection can be restored by normoglycemia, we treated rats with insulin. METHODS: Diabetic or nondiabetic rats were randomly subjected to 30-min ischemia/reperfusion, with ischemic postC or sevo-postC, with and without mitochondrial adenosine triphosphate-dependent potassium channel blocker 5-hydroxy decanoate sodium and PI3K antagonist wortmannin...
June 2011: Anesthesiology
Zhi Ye, Qulian Guo, E Wang, Min Shi, Yundan Pan
OBJECTIVE: To investigate whether the reactive oxygen species (ROS) and mitochondrial ATP-sensitive potassium (mitoKATP) channels were involved in delayed neuroprotection induced by sevoflurane on tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) levels. METHODS: Eighty-four male SD rats weighing 250 approximately 280 g, undergoing thread embolism of the right middle cerebral artery occlusion (MCAO) to cause focal ischemia for 2 h and then undergoing 24 h reperfusion, were randomly divided into 7 groups (n=12, each): a sham group(S), an ischemia-reperfusion group (I/R), a sevoflurane preconditioning group (Sevo), a 2-mercaptopropionylglycine (ROS scavenger)+sevoflurane group (MPG+Sevo), a 5-hydroxydecanoate (a mitoK(ATP) blocker) + sevoflurane group (5-HD+Sevo), an MPG group, and a 5-HD group...
February 2009: Zhong Nan da Xue Xue Bao. Yi Xue Ban, Journal of Central South University. Medical Sciences
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