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sevoflurane postconditioning

Kirsten F Smit, Daniel Brevoord, Stefan De Hert, Bas A de Mol, Raphaela P Kerindongo, Susan van Dieren, Wolfgang S Schlack, Markus W Hollmann, Nina C Weber, Benedikt Preckel
BACKGROUND: The noble gas helium induces pre- and postconditioning in animals and humans. Volatile anesthetics induce cardioprotection in humans undergoing coronary artery bypass graft (CABG) surgery. We hypothesized that helium induces pre- and postconditioning in CABG-patients, affecting signaling molecules protein kinase C-epsilon (PKC-ε), p38 mitogen activated protein kinase (p38 MAPK), extracellular signal-regulated kinase 1/2 (ERK-1/2) and heat shock protein 27 (HSP-27) within cardiac tissue, and reducing postoperative troponin levels...
October 14, 2016: Journal of Translational Medicine
Jin Yu, Yiliyaer Maimaitili, Peng Xie, Jianjiang Wu, Jiang Wang, Yining Yang, Haiping Ma, Hong Zheng
AIM: Hyperglycaemia-induced cell injury is a primary cause of cardiovascular complications in diabetic patients. In vivo studies demonstrated that sevoflurane postconditioning (SpostC) was cardioprotective against ischaemia/reperfusion injury, which was blocked by hyperglycaemia. This study investigated whether high glucose concentration abrogated SpostC cardioprotection in vitro by advancing mitochondrial fission and whether mitochondrial division inhibitor-1 (Mdivi-1) restored SpostC cardioprotection in cultured primary neonatal rat cardiomyocytes (NCMs)...
September 29, 2016: Acta Physiologica
Hyun-Chang Kim, Eugene Kim, Jung Il Bae, Kook Hyun Lee, Young-Tae Jeon, Jung-Won Hwang, Young-Jin Lim, Seong-Won Min, Hee-Pyoung Park
BACKGROUND: The antiapoptotic effects of sevoflurane postconditioning are responsible for neuroprotection against cerebral ischemia-reperfusion injury. Phosphorylation of the Janus family tyrosine kinases (JAK) 2-signal transducers and activators of transcription (STAT) 3 pathway is linked to antiapoptosis. Here, we determined whether the antiapoptotic effects of sevoflurane postconditioning are associated with activation of the JAK2-STAT3 pathway after global transient cerebral ischemia in rats...
June 22, 2016: Journal of Neurosurgical Anesthesiology
Sumin Gao, Zhengchao Yang, Ruili Shi, Dan Xu, Haobo Li, Zhengyuan Xia, Qing-Ping Wu, Shanglong Yao, Tingting Wang, Shiying Yuan
Sevofluane postconditioning (SPostC) protects heart against ischemia/reperfusion injury. However, SPostC cardioprotection is lost in diabetes whose cardiac heme oxygenase-1 (HO-1) is reduced. Brahma-related gene 1 (Brg1) facilitates nuclear factor-erythroid-2-related factor-2 (Nrf2) to activate HO-1 to increase myocardial antioxidant capacity in response to oxidative stress. However, cardiac Brg1 is reduced in diabetes. We hypothesized that SPostC confers cardioprotection by activating HO-1 through Nrf2/Brg1 and that impaired Nrf2/Brg1/HO-1 in diabetes is responsible for the loss of SPostC...
May 15, 2016: European Journal of Pharmacology
Jing-Jing Jiang, Chao Li, Heng Li, Lei Zhang, Zong-Hang Lin, Bao-Jun Fu, Yin-Ming Zeng
This study investigated the effect of sevoflurane postconditioning on post-ischaemic cardiac function, infarct size, myocardial mitochondrial ATP-sensitive potassium channel (mitoKATP) function and apoptosis in ageing rats to determine the possible mechanism underlying the cardioprotective property of sevoflurane. Ageing rat hearts were isolated and attached to a Langendorff apparatus. The hearts were then exposed or not to sevoflurane postconditioning in the presence or absence of 100 μmol/L 5-hydroxydecanoate (5-HD), a selective mitoKATP inhibitor...
May 2016: Clinical and Experimental Pharmacology & Physiology
Jiefu Lin, Tingting Wang, Yalan Li, Mengxia Wang, Haobo Li, Michael G Irwin, Zhengyuan Xia
The effect of sevoflurane postconditioning (sevo-postC) cardioprotection is compromised in diabetes which is associated with increased oxidative stress. We hypothesized that antioxidant N-Acetylcysteine may enhance or restore sevo-postC cardioprotection in diabetes. Control or streptozotocin-induced Type 1 diabetic rats were either untreated or treated with N-Acetylcysteine for four weeks starting at five weeks after streptozotocin injection and were subjected to myocardial ischemia-reperfusion injury (IRI), in the absence or presence of sevo-postC...
2016: Journal of Diabetes Research
Yuwen Zhang, Lei Zhang, Erwei Gu, Bingqing Zhu, Xianya Zhao, Jingjing Chen
Sufentanil, a commonly used opioid analgesic, could mimic ischemia postconditioning to attenuate ischemia reperfusion injury, but this effect might be hindered in diabetic animals by inhibition of glycogen synthase kinase-3β phosphorylation. Also, diabetes can abrogate the cardioprotection of sevoflurane (an inhaled anesthetic) against ischemia reperfusion injury, and short-term insulin treatment does not restore protection by sevoflurane postconditioning. We hypothesized that long-term insulin treatment might restore the cardioprotective effect of sufentanil postconditioning in diabetic rats via phosphorylation of glycogen synthase kinase-3β...
March 2016: Experimental Biology and Medicine
Zhongmeng Lai, Liangcheng Zhang, Jiansheng Su, Dongmiao Cai, Qingxiu Xu
BACKGROUND: Volatile anesthetic postconditioning has been documented to provide neuroprotection in adult animals. Our aim was to investigate whether sevoflurane postconditioning improves long-term learning and memory of neonatal hypoxia-ischemia brain damage (HIBD) rats, and whether the PI3K/Akt pathway and mitochondrial permeability transition pore (mPTP) opening participate in the effect. METHODS: Seven-day-old Sprague-Dawley rats were subjected to brain HI and randomly allocated to 10 groups (n=24 each group) and treated as follows: (1) Sham, without hypoxia-ischemia; (2) HI/Control, received cerebral hypoxia-ischemia; (3) HI+Atractyloside (Atr), (4) HI+Cyclosporin A (CsA), (5) HI+sevoflurane (Sev), (6) HI+Sev+ LY294002 (LY), (7) HI+Sev+ L-NAME (L-N), (8) HI+Sev+ SB216763 (SB), (9) HI+Sev+Atr, and (10) HI+Sev+CsA...
January 1, 2016: Brain Research
Peng Yu, Jing Zhang, Shuchun Yu, Zhenzhong Luo, Fuzhou Hua, Linhui Yuan, Zhidong Zhou, Qin Liu, Xiaohong Du, Sisi Chen, Lieliang Zhang, Guohai Xu
BACKGROUND AND PURPOSE: Myocardial infarction leads to heart failure. Autophagy is excessively activated in myocardial ischemia/reperfusion (I/R) in rats. The aim of this study is to investigate whether the protection of sevoflurane postconditioning (SPC) in myocardial I/R is through restored impaired autophagic flux. METHODS: Except for the sham control (SHAM) group, each rat underwent 30 min occlusion of the left anterior descending coronary (LAD) followed by 2 h reperfusion...
2015: PloS One
Yun-tai Yao, Ding-hua Liu, Li-huan Li
OBJECTIVE: To examine whether the combination of anesthetic preconditioning and anesthetic postconditioning could elicit additional cardio-protection as compared to either anesthetic preconditioning or anesthetic postconditioning alone and its underlying mechanism. METHODS: Isolated rat hearts were randomized into one of four groups: CTRL group (30 min of ischemia followed by 120 min of reperfusion alone); SpreC group (3% sevoflurane preconditioning was administered for 15 min followed by 10 min of washout before ischemia); SpostC group (3% sevoflurane postconditioning was administered during the first 15 min of reperfusion after ischemia); SpreC+SpostC group (the protocols of SpreC and SpostC were combined)...
March 2016: Perfusion
Jing Zhang, Chen Wang, Shuchun Yu, Zhenzhong Luo, Yong Chen, Qin Liu, Fuzhou Hua, Guohai Xu, Peng Yu
Phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) pathway plays a key role in myocardial ischemia-reperfusion (I/R) injury. Mammalian target of rapamycin (mTOR), a downstream target of PI3K/AKT signaling, is necessary and sufficient to protect the heart from I/R injury. Inhaled anesthetic sevoflurane is widely used in cardiac surgeries because its induction and recovery are faster and smoother than other inhaled anesthetics. Sevoflurane proved capable of inducing postconditioning effects in the myocardium...
2014: Scientific Reports
Jason A Bartos, Timothy R Matsuura, Mohammad Sarraf, Scott T Youngquist, Scott H McKnite, Jennifer N Rees, Daniel T Sloper, Frank S Bates, Nicolas Segal, Guillaume Debaty, Keith G Lurie, Robert W Neumar, Joseph M Metzger, Matthias L Riess, Demetris Yannopoulos
OBJECTIVE: Ischemic postconditioning (stutter CPR) and sevoflurane have been shown to mitigate the effects of reperfusion injury in cardiac tissue after 15min of ventricular fibrillation (VF) cardiac arrest. Poloxamer 188 (P188) has also proven beneficial to neuronal and cardiac tissue during reperfusion injury in human and animal models. We hypothesized that the use of stutter CPR, sevoflurane, and P188 combined with standard advanced life support would improve post-resuscitation cardiac and neurologic function after prolonged VF arrest...
February 2015: Resuscitation
Matthias L Riess, Timothy R Matsuura, Jason A Bartos, Martin Bienengraeber, Mohammed Aldakkak, Scott H McKnite, Jennifer N Rees, Tom P Aufderheide, Mohammad Sarraf, Robert W Neumar, Demetris Yannopoulos
BACKGROUND: Anaesthetic postconditioning (APoC) attenuates myocardial injury following coronary ischaemia/reperfusion. We hypothesised that APoC at the initiation of cardiopulmonary resuscitation (CPR) will improve post resuscitation myocardial function along with improved mitochondrial function in a pig model of prolonged untreated ventricular fibrillation. METHODS: In 32 pigs isoflurane anaesthesia was discontinued prior to induction of ventricular fibrillation that was left untreated for 15 min...
December 2014: Resuscitation
Bo Li, Jian Sun, Guoyi Lv, Yonghao Yu, Guolin Wang, Keliang Xie, Yang Jiao, Yang Yu
Oxidative damage plays a critical role in many diseases of the central nervous system. This study was conducted to determine the molecular mechanisms involved in the putative anti-oxidative effects of sevoflurane against experimental stroke. Focal cerebral ischemia was performed via 1h of middle cerebral artery occlusion followed by reperfusion. At the onset of reperfusion, rats were subjected to postconditioning with sevoflurane or without sevoflurane for 1h. Neurological deficit score was assessed at different time points after reperfusion...
November 2014: International Journal of Developmental Neuroscience
Jun-Kuan Wang, Hui-Fang Wu, Hui Zhou, Bo Yang, Xian-Zhi Liu
OBJECTIVES: Postconditioning with sevoflurane has been shown to protect against focal cerebral ischemia and reperfusion injury. However, the mechanism remains elusive. In this study, we tested the hypothesis that mitochondrial ATP-sensitive potassium (mitoKATP) and mitochondrial permeability transition pore (mPTP) play roles in the neuroprotection of postconditioning with sevoflurane. METHODS: Adult male Sprague-Dawley rats were subjected to MCAO for 90 minutes and then treated with sevoflurane at the beginning of reperfusion...
January 2015: Neurological Research
P Dong, J Zhao, Y Zhang, J Dong, L Zhang, D Li, L Li, X Zhang, B Yang, W Lei
Aging is associated with exacerbated brain injury after ischemic stroke. Herein, we explored the possible mechanisms underlying the age-associated exacerbated brain injury after ischemic stroke and determined whether therapeutic intervention with anesthetic post-conditioning would provide neuroprotection in aged rats. Male Fisher 344 rats (young, 4 months; aged, 24 months) underwent 2h of middle cerebral artery occlusion (MCAO) followed by 24-h reperfusion, with or without sevoflurane post-conditioning for 15 min immediately at the onset of reperfusion...
September 5, 2014: Neuroscience
Yu-Lin Zhang, Yun-Tai Yao, Neng-Xin Fang, Cheng-Hui Zhou, Jun-Song Gong, Li-Huan Li
AIM: Sevoflurane postconditioning (SpostC) has been shown to protect the heart from ischemia-reperfusion (I/R) injury. In this study, we examined whether SpostC affected autophagic flux in myocardial tissues that contributed to its cardioprotective effects in rats following acute I/R injury. METHODS: SD rats underwent 30 min of left anterior descending coronary artery ligation followed by 120 min of reperfusion. The rats were subjected to inhalation of 2.4% (v/v) sevoflurane during the first 5 min of reperfusion, and chloroquine (10 mg/kg, ip) was injected 1 h before I/R...
June 2014: Acta Pharmacologica Sinica
Xiaoyan Ren, Zhi Wang, Hong Ma, Zhiyi Zuo
Application of volatile anesthetics after brain ischemia provides neuroprotection in adult animals (anesthetic postconditioning). We tested whether postconditioning with sevoflurane, the most commonly used general anesthetic in pediatric anesthesia, reduced neonatal brain injury in rats. Seven-day-old Sprague-Dawley rats were subjected to brain hypoxia-ischemia (HI). They were postconditioned with sevoflurane in the presence or absence of 5-hydroxydecanoic acid, a mitochondrial KATP channel inhibitor. Sevoflurane postconditioning dose-dependently reduced brain tissue loss observed 7 days after brain HI...
September 2014: Neurological Sciences
Chenghui Zhou, Huatong Li, Yuntai Yao, Lihuan Li
Although both sevoflurane postconditioning (SPoC) and delayed remote ischemic preconditioning (DRIPC) have been proved effective in various animal and human studies, the combined effect of these 2 strategies remains unclear. Therefore, this study was designed to investigate this effect and elucidate the related signal mechanisms in a Langendorff perfused rat heart model. After 30-minute balanced perfusion, isolated hearts were subjected to 30-minute ischemia followed by 60-minute reperfusion except 90-minute perfusion for control...
November 2014: Journal of Cardiovascular Pharmacology and Therapeutics
Jan Stumpner, Tobias Tischer-Zeitz, Anja Frank, Christopher Lotz, Andreas Redel, Markus Lange, Franz Kehl, Norbert Roewer, Thorsten Smul
Cyclooxygenase (COX)-2 mediates ischemic pre- and postconditioning as well as anesthetic-induced preconditioning. However, the role of COX-1 and -2 in anesthetic-induced postconditioning has not been investigated. We evaluated the role of COX-1 and -2 in sevoflurane-induced postconditioning in vivo. Pentobarbital-anaesthetized male C57BL/6 mice were subjected to 45 minutes of coronary artery occlusion and 3 hours of reperfusion. Animals received either no intervention, the vehicle dimethyl sulfoxide (DMSO, 10 µL/g intraperitoneally), acetylsalicylic acid (ASA, 5 µg/g intraperitoneally), the selective COX-1 inhibitor SC-560 (10 µg/g intraperitoneally), or the selective COX-2 inhibitor NS-398 (5 µg/g intraperitoneally)...
September 2014: Seminars in Cardiothoracic and Vascular Anesthesia
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