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LIAO Jin-hua LI Jian-ling YAN Yan-nian LI Ya-lan HU Dong-hua XIANG Ming-fang HUANG Qiang MO Shi-huang PENG Xue-mei WANG Xiao-ping 《园艺学报》2011,27(8):1476-1484
AIM: To investigate the effects of sevoflurane preconditioning on the production of reactive oxygen species (ROS) and nitric oxide (NO), the activity of superoxide dismutase(SOD), glutathione peroxide(GPx) and catalase(CAT) in myocardial ischemia-reperfusion injury(IRI). METHODS: Sixty rats were randomly allocated to 8 groups. Following 2% sevoflurane preconditioning for 30 min, the left anterior descending artery was ligated for 30 min and then reperfused for 120 min in vivo. The infarction size of the hearts was measured with the staining of 2,3,5-triphenyltetrazoliumchloride. The myocardial apoptotic index was measured by the method of TUNEL. The ROS fluorescent probe dihydroethidium was used for the measurement of ROS. The myocardium was homogenized for the measurement of NO, SOD, GPx and CAT. To evaluate the effects of ROS and NO on the cardioprotection of sevoflurane preconditioning, ROS scavenger N-(2-mercaptopropionyl) glycine (2-MPG) or NOS inhibitor Nω-nitro-L-arginine methyl ester (L-NAME) were employed to block their actions. RESULTS: Compared with control group, the production of ROS was induced by sevoflurane preconditioning before ischemia-reperfusion injury (12.0±0.8 vs 2.6±0.5, P<0.05) and decreased after ischemia-reperfusion injury (16.2 ±0.9 vs 24.9±1.3, P<0.05). 2-MPG decreased the elevation of ROS caused by sevoflurane preconditioning before ischemia-reperfusion injury (5.1±0.7 vs 12.0±0.8, P<0.05). No difference of ROS production between treating with 2-MPG+Sevo+IRI and with IRI (24.9±1.4 vs 24.9±1.3, P>0.05) was observed. Compared with control group, sevoflurane preconditioning also induced the generation of NO (34.5±3.2 vs 15.9±1.4, P<0.05) and the activity of SOD(1.5±0.5 vs 0.6±0.2, P<0.05), GPx(22.8±2.5 vs 12.7±2.2, P<0.05) and CAT(15.5±1.8 vs 11.2±1.4, P<0.05). 2-MPG blocked the increase in NO production and inhibited the activity of SOD,GPx,CAT. L-NAME also attenuated the activity of SOD,GPx,CAT. CONCLUSION: Sevoflurane preconditioning protects the rat heart against ischemia-reperfusion injury by reducing the infarction size and apoptosis. Production of ROS at sub-injury dose induced by sevoflurane preconditioning stimulates the myocardium to create SOD,GPx,CAT and NO, thus inhibiting the further formation of ROS and protecting the heart under the condition of ischemia-reperfusion. 相似文献
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The effects of sevoflurane or isoflurane on arterial blood gas, arterial oxyhaemoglobin saturation and end-tidal CO2 tension were monitored during induction and maintenance of anaesthesia in 10 premedicated New Zealand White (NZW) rabbits.For induction, the anaesthetic agents were delivered via a face-mask. After induction was completed, an endotracheal tube was introduced for maintenance of anaesthesia for a period of 90 minutes. Changes in heart rate, respiratory rate, arterial blood gas, arterial oxyhaemoglobin saturation, blood pH and end-tidal CO2 tension were recorded. Although sevoflurane and isoflurane produce similar cardiopulmonary effects in premedicated rabbits, sevoflurane provides a smoother and faster induction because of its lower blood/gas partition coefficient. Thus sevoflurane is probably a more suitable agent than isoflurane for mask induction and maintenance. Its lower blood solubility also makes sevoflurane more satisfactory than isoflurane for maintenance of anaesthesia because it allows the anaesthetist to change the depth of anaesthesia more rapidly. 相似文献
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AIM: To investigate the effect of sevoflurane (Sevo) on the dendritic development in prefrontal cortex (PFC) of neonatal rats and the role of cyclin dependent kinase 5 (Cdk5)- collapsin response mediator protein (CRMP) pathway in it. METHODS: Eighty-eight postnatal day 7 Sprague Dawley (SD) rats were randomly divided into 4 groups (n=22): Air+NS group, Air+roscovitine (Ros) group, Sevo+NS group and Sevo+Ros group. The rats in Air+NS group and Air+Ros group were exposed to the air for 4 h, while the rats in the other 2 groups were exposed to 2.8% sevoflurane for 4 h. The rats received intraperitoneal injection of 150 μL normal saline 15 min before exposure in the Air+NS group and Sevo+NS group, while the rats in the Air+Ros group and Sevo+Ros group received intraperitoneal injection of 150 μL roscovitine (in DMSO solution, 10 mg/kg) 15 min before exposure. At the end of exposure, the cortices of the rat brain were collected and the protein levels of P35, P25, Cdk5, CRMP1, CRMP2, CRMP4 and p-CRMP2 Ser522 in PFC were detected by Western blot. On the postnatal day 30, the rat brains were sectioned for Golgi-Cox staining and morphological analysis of dendrites in the PFC neurons. Open-field test and contextual fear conditioning test were performed on postnatal days 25~27 and 31~32, respectively. RESULTS: Compared with Air+NS group, the expression of P35 in the Sevo+NS group was significantly decreased, and the expression of P25 was dramatically increased (P <0.05), whereas roscovitine partly reversed the changes above induced by sevoflurane (P <0.05). The expression of Cdk5 was not significantly different among all groups. Compared with the Air+NS group, the expression of CRMP1, 2, and 4 in the Sevo+NS group were decreased, and the protein level of p-CRMP2 Ser522/CRMP2 was increased (P <0.05), whereas roscovitine partly reversed the changes above induced by sevoflurane (P <0.05), except for the expression of CRMP2. Compared with Air+NS group, the total dendrite length, secondary dendritic length and interactions on 60 and 80 μm shells in the Sevo+NS group were decreased (P <0.01), whereas roscovitine partly reversed the changes above induced by sevoflurane (P <0.05). Compared with Air+NS group, the percentage of freezing time in the Sevo+NS group was decreased (P <0.01), whereas roscovitine partly reversed the changes induced by sevoflurane (P <0.05). No significant difference among groups in the open-field test was observed. CONCLUSION: Sevoflurane exposure disturbed dendritic development of neurons in PFC, learning and memory ability of neonatal rats, which may be mediated by Cdk5-CRMP pathway. 相似文献
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七氟醚氟烷异氟醚对犬心脏功能影响的临床比较 总被引：2，自引：2，他引：0
为评价七氟醚对心脏功能的影响。并与氟烷和异氟醚作比较，对动物医院就诊、心肺功能正常、拟作手术治疗的8例患犬进行麻醉试验，所有犬均以l-美散痛和安定和为麻醉前给药，分别以1.5%七氟醚、1.0%七氟醚与66.7%笑气、1.0%氟烷、1.5%异氟醚维持手术麻醉，并作人工呼吸，各组均未观察到心律异常，手术麻醉期间，七氟醚组犬心率降幅（4.73%）低于异氟醚组（9.74%)或氟烷组（10.23%)。七氟醚组、氟烷组和异氟醚组的收缩压/舒张压轻度升高（七氟醚3.38%/11.93%氟烷6.09%/9.09%，异氟醚4.82%/6.25%)。而七氟醚与笑气组的收缩压/舒张压则降低（6.84%/5.73%)。证实七氟醚应为临床首选的吸入麻醉剂。 相似文献
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LI Heng YANG Cheng-xiang SUN Kai MENG Xian-hui DONG Xiao-li ZENG Yin-ming WANG Jun 《园艺学报》2007,23(10):1891-1895
AIM: To investigate the effect of volatile anesthetics on function,metabolism,ATPase activity and free radicals in isolated ischemia /reperfusion (I/R) rat hearts.METHODS: 136 SD rats were anesthetized with pentobarbital and randomly divided into six groups and 17 sub-groups (n=8),according to the given drug.In a normal thermal isolated Langendorff rat heart model,four volatile anesthetics in 1.5 MAC concentration were given before global ischemia 25 min and during reperfusion 30 min.Coronary flow (CF),LVEDP,left ventricular developed pressure (LVDP),±dp/dt were monitored at 15 min of equilibrium,15 min of drug treatment,the end of reperfusion.Myocardial adenosine triphosphate (ATP),malodialdehyde (MDA),activity of Ca2＋-ATPase and Na＋-K＋-ATPase,and superoxide dismutase (SOD) were determined at 15 min of equilibrium,15 min of drug treatment or absence,10 min global ischemia and the end of reperfusion.RESULTS: CF and LVEDP were increased significantly after exposured to volatile anesthetics 15 min,and LVDP,+dp/dtmax were significantly decreased.However,LVDP and +dp/dtmax were increased at the end of reperfusion in the treated groups.HR in halothane and isoflurane groups was decreased before ischemia and after reperfusion.The myocardial ATP content was significantly increased before and after ischemia in the treated groups.At the end of reperfusion,the activity of SOD was significantly higher and myocardial MDA content was significantly lower in the treated groups than those in control group.The activity of Ca2＋-ATPase,compared with the control group,was markedly decreased before ischemia in halothane,enflurane and isoflurane group.Nonetheless,the activity of Ca2＋-ATPase was clearly increased in the treated groups during ischemia and at the end of reperfusion.The activity of Na＋-K＋-ATPase was only enhanced in halothane group at the end of reperfusion among groups.CONCLUSION: The volatile anesthetics depress myocardial systolic function.There are markedly protective effects against myocardial I/R injury.Meanwhile,the volatile anesthetics improve the recovery of function and metabolism,and increase CF and the activity of Ca2＋-ATPase and Na＋-K＋-ATPase in rats. 相似文献
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LI Jian-ling ZHU Xiao-qing LI Xue-min LI Hong-mei WANG Yan-ping WANG Yuan QI Ren-bin LI Ya-lan 《园艺学报》2012,28(8):1410-1414
AIM:To investigate the effects of sevoflurane(Sevo) preconditioning on myocardial dysfunction in lipopolysaccharide(LPS)-challenged mice. METHODS:Forty male BALB/c mice were randomly allocated to 4 groups:control group, LPS group, Sevo+LPS group and Sevo group. Following pretreatment with or without 2% Sevo for 30 min and washing out for 10 min, all mice received intraperitoneal injection of LPS or normal saline(NS). The mice received an echocardiographic evaluation by a high-resolution in vivo imaging system 12 h after administration of LPS or NS. The mice were then killed and the hearts were removed for histological analysis. Serum levels of lactic dehydrogenase(LDH), creatine kinase-MB(CK-MB) were measured with an automatic biochemical analyzer. The myocardium was homogenized for detecting the activity of inducible nitric oxide synthase(iNOS) and the content of nitric oxide(NO). RESULTS:Echocardiographic evaluation demonstrated that LPS resulted in an increase in lert ventricular end-diastolic volume and significant decreases in stroke volume,cardiac output and ejection fraction. The alteration of cardiac functions was inhibited by the pretreatment with Sevo. LPS caused significant elevation of LDH and CK-MB in serum samples and severe pathological damage of the hearts. Compared with LPS group, serum levels of LDH and CK-MB were reduced and pathological damage was attenuated in Sevo+LPS group. Sevo preconditioning also significantly attenuated the increases in iNOS and NO induced by LPS. CONCLUSION:Sevo preconditioning protects against myocardial impairment and myocardial dysfunction in LPS-challenged mice. Inhibition of iNOS activity and of NO production by Sevo preconditioning may contribute to the beneficial role in the process of cardioprotection during endotoxemia. 相似文献
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WANG Meng-xia LI Jian-ling LIANG Zhao-jia ZHONG Zhao HU Dong-hua WANG Fei-fei TIAN He GAO Lan LI Ya-lan 《园艺学报》2017,33(11):1932-1937
AIM: To observe the effects of sevoflurane preconditioning on brain injury in hypoxic mice and its possible mechanism. METHODS: Male C57BL/6J mice were randomly divided into control (C) group, hypoxia (H) group, 2% sevoflurane preconditioning for 30 min + hypoxia (S1+H) group, 2% sevoflurane preconditioning for 60 min+hypoxia (S2+H) group and 4% sevoflurane preconditioning for 30 min + hypoxia (S3+H) group. The hypoxia model was established by continuous inhalation of (6.5±0.1)% O2 for 24 h. The sevoflurane preconditioning treatments, S1, S2 and S3, were conducted by inhalation of 2% sevoflurane for 30 min, 2% sevoflurane for 60 min and 4% sevoflurane for 30 min, respectively, with the carrier of (21.0±0.5)% O2, followed by washout for 15 min and then hypoxia treatment. The histological changes of the hippocampal CA1 area were observed under light microscope and transmission electron microscope (TEM), and serum lactate dehydrogenase (LDH) activity was measured by colorimetric method. Furthermore, the protein levels of erythropoietin (EPO) and vascular endothelial growth factor (VEGF) in brain tissue homogenate were examined by ELISA, and the content of malondialdehyde (MDA) and the activity of superoxide dismutase (SOD) and glutathione peroxidase (GPx) were measured by microplate reader. RESULTS: After hypoxia for 24 h, cell edema or pyknosis in the hippocampal CA1 area was observed in H group. Sevoflurane preconditioning reduced hypoxic injury, and the cell ultrastructure under TEM was significantly improved in S2+H group. Compared with C group, the serum LDH activity and the levels of EPO, VEGF and MDA in brain tissues were significantly increased in H group, while the activity of SOD and GPx decreased. After sevoflurane pretreatment, the serum LDH activity and the levels of EPO and VEGF in brain tissues were lower than those in H group, and the most significant difference was observed in S2+H group. Moreover, the MDA content and SOD activity decreased, and the GPx activity increased in the sevoflurane preconditioning groups. CONCLUSION: Sevoflurane preconditioning attenuates brain injury in hypoxic mice by regulating antihypoxic protein synthesis and reducing oxidative stress. 相似文献
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为评价七氟醚对肝肾功能的影响，并与氟烷和异氟醚作比较，对动物医院就诊的心肺功能正常，拟作手术治疗的61头患犬进行麻醉试验，所有犬均以l-美散痛和安定作为麻醉前给药。分别以1．5％七氟醚、1．0％氟烷、1．5％异氟醚维持手术麻醉，所有3组中无一组可见肝肾毒性副作用。至七氟醚麻醉后48h，GLDH，AST，ALT，γ-GT，总胆红素，AP，尿素氮和肌酐显示正常。 相似文献
10.
AIM: To investigate the effects of isoflurane and sevoflurane at the same dose on apoptosis of cortical neuron in neonatal rats and the role of mitogen-activated protein kinases (MAPKs) pathway.METHODS: Eleven neonatal rats were selected at postnatal day 7 from 1 litter (altogether 5 litters) and assigned randomly into control group (C group), isoflurane group (Ⅰ group) and sevoflurane group (S group). The rats in Ⅰ group, S group or C group were exposed to 1.1% isoflurane, 1.8% sevoflurane and room air for 4 h, respectively. The brain of neonatal rats were perfused and embedded by paraffin. Caspase-3 positive expression in the retrosplenial cortex (RS) of the brain was observed by immunohistochemical staining. Meanwhile, the fresh cortex was separated at 0 h in C group and at 2 h and 4 h in Ⅰ group and S group. The levels of phospho-SAPK/JNK and SAPK/JNK, phospho-p38 and p38 in fresh cortex were detected by Western blotting.RESULTS: Caspase-3 positive cells in the the cortex were increased by 441% in Ⅰ group (P<0.01) and 151% in S group (P<0.01) as compared to C group, and increased by 115% in Ⅰ group (P<0.05) as compared to S group. The protein levels of phospho-SAPK/JNK in the cortex were increased by 219% at 2 h (P<0.05) and 181% at 4 h (P<0.05) in Ⅰ group, while no significant difference between S group and C group was observed. The phospho-p38 protein in the cortex was increased by 38.9% at 2 h (P<0.05) and 36.9% at 4 h (P<0.05) in Ⅰ group, and increased by 32.6% (P<0.05) at 2 h and 128.0% at 4 h (P<0.01) in S group as compared to C group.CONCLUSION: Isoflurane induces more apoptotic neurons in the cortex of the brain in neonatal rats at postnatal day 7 than sevoflurane. Isoflurane induces apoptosis mainly by activating SAPK/JNK phosphorylation, while sevoflurane induces aopotosis by activating p38 phosphorylation. 相似文献