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1. Emulsified isoflurane preconditioning protects cardiac toxicity induced by bupivacaine | |||
ZHOU Cheng,HUANG Han,LIU Jin | |||
Clinical Medicine 21 April 2017 | |||
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Abstract:Lipid emulsion has been identified as a potent rescuing agent for cardiac arrest caused by local anesthetic overdose. In this animal study, we investigated weather prophylactic infusion of emulsified isoflurane, a mixture of lipid emulsion and isoflurane, could increase the tolerability for bupivacaine-induced cardiac toxicity. Rats were randomly assigned to receive one of the following treatments: saline, 30% Intralipid, 4% Emulsified Isoflurane (4% EISO), 2% EISO, 0.5% propofol, 0.25% propofol, inhaled isoflurane plus 30% Intralipid, or inhaled isoflurane plus saline, for 15 min. Then 0.75% bupivacaine was infused at the rate of 8ml/kg/min. The time needed to induce cardiac arrest was recorded and the bupivacaine dose was calculated. Another set of rats were intubated for mechanical ventilation and catheterized for invasive arterial pressure monitoring while receiving one of the following sedative pretreatments for 15 min: 4% EISO, 0.5% propofol, inhaled isoflurane plus saline, or inhaled isoflurane plus 30% Intralipid. Then bupivacaine was infused at the rate of 8ml/kg/min for 120 seconds (sublethal dose). The hemodynamic parameters were recorded till circulation fully recovered. Pretreatment with 4% EISO significantly increased the dose of bupivacaine required to induce cardiac arrest (68.69±7.57mg/kg vs. 26.61±5.13mg/kg for saline, p <0.01). Prophylactic infusion of Intralipid alone also increased the bupivacaine tolerability (51.41±9.68 mg/kg, p<0.05 vs. saline), but less efficient than 4% EISO (p<0.05 vs. 4% EISO). Pretreatments with 4% EISO provided best preservation of hemodynamic parameters in the face of circulatory fluctuation caused by sublethal dose of bupivacaine. 4% emulsified isoflurane preconditioning significantly increases the threshold of bupivacaine-induced cardiac arrest in rats and prevents circulatory instability caused by sublethal dose of bupivacaine. Our results implicate the potential application of emulsified isoflurane as an adjuvant agent in local anesthesia. | |||
TO cite this article:ZHOU Cheng,HUANG Han,LIU Jin. Emulsified isoflurane preconditioning protects cardiac toxicity induced by bupivacaine[OL].[21 April 2017] http://en.paper.edu.cn/en_releasepaper/content/4727694 |
2. Emulsified Isoflurane Produces Cardiac Protection in a Dog Cardiopulmonary Bypass Model by Adding to Cardioplegia Solution | |||
HUANG Han,ZHOU Cheng,LIU Jin | |||
Clinical Medicine 21 April 2017 | |||
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Abstract:This study investigated whether caridoplegia solution with Emulsified Isoflurane (EI) could improve cardiaoprotection in a dog CPB model of great similarity to clinical settings. Adult dogs were randomly assigned to receive one of the following cardioplegia solutions: St. Thomas with EI (group ST+EI), St. Thomas with 30% Intralipid (group ST+EL) and St. Thomas alone (group ST). The aorta was crossclamped for two hours followed by reperfusion for another two hours, during which cardiac output was measured and dosages of positive inotropic agent to maintain normal hemodynamics were recorded. Serum level of cardiac troponin I (cTnI) and CK-MB were measured. Deletion of cardiac mitochondrial DNA was examined at the end of reperfusion. Compared with ST, ST+EI decreased the requirement of dopamine support while animals receiving ST+EI had a significantly larger cardiac output. ST+EI reduced post-CPB release of cTnI and CK-MB. Mitochondrial DNA loss was observed in only one of the tested animals from group ST+EI while it was seen in all the tested animals from group ST+EL and ST. Addition of emulsified isoflurane into cardioplegia solution protects against myocardial ischemia reperfusion injury. This protective effect might be mediated by preserving mitochondrial ultrastructure and DNA integrity. | |||
TO cite this article:HUANG Han,ZHOU Cheng,LIU Jin. Emulsified Isoflurane Produces Cardiac Protection in a Dog Cardiopulmonary Bypass Model by Adding to Cardioplegia Solution[OL].[21 April 2017] http://en.paper.edu.cn/en_releasepaper/content/4727672 |
3. Edaravone protects the neural stem cell proliferation under hypoxia in vitro | |||
LEI Shan,ZHANG Pengbo,LI Weisong,GAO Ming,HE Xijing,ZHENG Juan,LI Xu,WANG Xiao,WANG Ning,ZHANG Junfeng,QI Cunfang,LV Haixia,CHEN Xinlin,LIU Yong | |||
Clinical Medicine 10 January 2014 | |||
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Abstract:Hypoxia stimulates neural stem cell (NSC) proliferation and enhances generation of endogenous reactive oxygen species (ROS). However, the role of edaravone in NSC proliferation under severe hypoxia remains unclear. We used a free radical scavenger edaravone to investigate the effect and underlying mechanism of edaravone on NSC proliferation under 0.3% oxygen condition. Neural stem cells (NSCs) were prepared from 14-day embryonic mice and identified by immunohistochemical analysis. NSCs were incubated with edaravone (0μM or 100 μM) for 24 h under hypoxia (0.3% oxygen) or normoxia (5% CO2/95% air), respectively. Cell proliferation was evaluated by 5'-bromo-2'-deoxyuridine (BrdU) incorporation. ROS were detected by 2,7-dichlorofluorescien diacetate (DCF-DA) assay. Cell apoptosis was assessed by flow cytometric analysis and terminal dUTP nick-end labeling. HIF-1α and activated caspase-3 proteins were quantified by western blot analysis. After 24 hours of hypoxia, most cells were nestin and HIF-1α positive. Hypoxia increased ROS generation, elevated protein levels of HIF-1α and activated caspase-3, and facilitated NSC apoptosis compared with normoxia (P < 0.01), respectively. Treatment with edaravone, a free radical scavenger, inhibited significantly the above changes induced by hypoxia (P < 0.01). Edaravone also increased significantly NSC proliferation under hypoxia (P < 0.01). These findings indicate that edaravone promotes NSC proliferation under 0.3% oxygen condition probably by inhibiting HIF-1α, caspase -3 and apoptosis under severe hypoxia. The present data reveal a novel ROS-dependent HIF-1α-mediated caspase-3 activation pathway which leads to NSC apoptosis in vitro. | |||
TO cite this article:LEI Shan,ZHANG Pengbo,LI Weisong, et al. Edaravone protects the neural stem cell proliferation under hypoxia in vitro[OL].[10 January 2014] http://en.paper.edu.cn/en_releasepaper/content/4581610 |
4. Pre- and post-treatment with edaravone protects CA1 hippocampus and enhances neurogenesis in the subgranular zone of dentate gyrus after transient global cerebral ischemia in rats | |||
LEI Shan,ZHANG Pengbo,LI Weisong,GAO Ming,HE Xijing,ZHENG Juan,LI Xu,WANG Ning,WANG Xiao,ZHANG Junfeng,QI Cunfang,LV Haixia,CHEN Xinlin,LIU Yong | |||
Clinical Medicine 10 January 2014 | |||
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Abstract:Edaravone is clinically used for treatment of patients with acute cerebral infarction. However, the effect of edaravone on neurogenesis in the hippocampus following ischemia remains unknown. In the present study, we explored whether pre- and post- treatment of edaravone had any effect on neural stem/progenitor cells (NSPCs) in the subgranular zone (SGZ) of hippocampus in a rat model of transient global cerebral ischemia. Male Sprague-Dawley rats were divided into 3 groups, sham-operated (n = 15), control (n = 15), and edaravone-treated (n = 15) groups. Newly-generated cells were labeled by 5-bromo-2-deoxyuridine (BrdU). Immunohistochemistry was used to detect neurogenesis in the SGZ at 7, 14 and 21 d following ischemia. Terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) was used to detect cell apoptosis. Our results indicate that pre- and post-treatment with edaravone enhances neurogenesis and protects NSPCs from apoptosis in the hippocampus.? | |||
TO cite this article:LEI Shan,ZHANG Pengbo,LI Weisong, et al. Pre- and post-treatment with edaravone protects CA1 hippocampus and enhances neurogenesis in the subgranular zone of dentate gyrus after transient global cerebral ischemia in rats[OL].[10 January 2014] http://en.paper.edu.cn/en_releasepaper/content/4581616 |
5. Polymerized human placenta hemoglobin given before ischemia protects rat heart from ischemia reperfusion injury | |||
Li Tao,Zhou Ronghua,Wu Wei,Xiang Xujin,Zhu Da,Yang Chengmin,Li Yanyan,Liu Jin | |||
Clinical Medicine 16 August 2011 | |||
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Abstract:This study was to investigate whether polymerized human placenta hemoglobin (PolyPHb) given before ischemia protects in vivo rat heart function against ischemia/reperfusion (I/R) injury. Forty-five male Sprague-Dawley rats were randomly divided (n=15 per group) to sham group, control group (pretreatment with Lactated Ringer's solution) or PolyPHb group (pretreatment with 0.1gHb/kg PolyPHb). Rat hearts were subjected to 30-min ischemia by occlusion of left anterior descending, followed by 2-hr reperfusion. As compared to the control group, PolyPHb preserved cardiac function and reduced cardiac troponin-I release and histopathological changes. Therefore, PolyPHb pretreatment provided a profound cardioprotective effect on in vivo rat heart. | |||
TO cite this article:Li Tao,Zhou Ronghua,Wu Wei, et al. Polymerized human placenta hemoglobin given before ischemia protects rat heart from ischemia reperfusion injury[OL].[16 August 2011] http://en.paper.edu.cn/en_releasepaper/content/4439184 |
6. Reversible Conduction Block in Isolated Toad Sciatic Nerve by Emulsified Isoflurane | |||
Li Zhuo,Yang Jing ,Liu Jin ,Gong Chunyu ,Gan Jing ,Zhang Xian ,Luo Wenjun ,Li Guohua | |||
Clinical Medicine 25 December 2009 | |||
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Abstract:Background: Studies have shown that the local use of volatile anesthetics can produce some local anesthetic effects. The present study was designed to evaluate characteristics of nerve conduction block of emulsified isoflurane (EI), and compare its nerve blockade with 1% lidocaine, by measuring compound nerve action potential (CNAP) parameters in isolated toad sciatic nerve. Methods: One hundred isolated toad sciatic nerves were selected and randomly assigned to 10 groups of 10 each, receiving administration of 2-8% EI (v/v) (EI8 group, etc), 1% lidocaine (Lido group), 30% Intralipid?(Lipid group) and Ringer?solution (RS group) for 10min, respectively. Then all nerves were washed and soaked by RS for 10min and 30min. The nerve conduction block effect was represented by CNAP parameters which were recorded by extracellular recording technique per min. Results: The results showed that the negative amplitudes of CNAP were decreased by EI as well as Lidocaine (P < 0.05), and the conduction velocities of CNAP were also decreased in some time points (D7-W3) (P < 0.05). After RS washing, the two parameters recovered gradually. The changes in the two parameters induced by EI had slower onset rates and faster recoveries than those produced by lidocaine (7 min vs. 1 min, 9 min vs. 30 min). The nerve blockade induced by EI was dose-dependent (P < 0.05), and the half maximal inhibition concentration of EI was 5.46 %. Conclusions: EI produced completely reversible and dose-dependent nerve conduction inhibition, which had slower onset and faster recovery compared to those produced by lidocaine. | |||
TO cite this article:Li Zhuo,Yang Jing ,Liu Jin , et al. Reversible Conduction Block in Isolated Toad Sciatic Nerve by Emulsified Isoflurane[J]. |
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