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Objective To evaluate the role of cholinergic anti-inflammatory pathway in dexmedeto-midine pretreatment-induced reduction of acute lung injury in a rat model of intestinal ischemia-reperfusion ( I∕R) . Methods Twenty-four healthy male Sprague-Dawley rats, aged 2-3 months, weighing 200-250 g, were divided into 4 groups ( n=6) using a random number table method: sham operation group ( S group) , intestinal I∕R group ( II∕R group ) , dexmetomidine group ( DEX group) and α7 nicotinic acetyl-choline receptor antagonistα-bungarotoxin (α-BGT) group (α-BGT group) . Intestinal I∕R was produced by occlusion of the superior mesenteric artery ( SMA) for 60 min followed by 120 min of reperfusion in anesthe-tized rats. Dexmetomidine 5 μg·kg-1 ·h-1 was injected via the tail vein at 1 h before operation in DEX group andα-BGT group. α-BGT 1μg∕kg was intraperitoneally injected at 15 min before dexmetomidine in-jection in α-BGT group. Rats were sacrificed at 120 min of reperfusion, and lung tissues were obtained for microscopic examination of pathological changes ( with a light microscope) and for determination of wet∕dry weight ratio ( W∕D ratio) , tumor necrosis factor-alpha ( TNF-α) and interleukin-6 ( IL-6) contents ( using enzyme-linked immunosorbent assay) , malondialdehyde ( MDA) content ( using thiobarbital acid method) and superoxide dismutase ( SOD) activity ( by xanthine oxidase method) . Results Compared with group S, the W∕D ratio and contents of MDA, TNF-αand IL-6 were significantly increased, and the SOD activi-ty was decreased in II∕R and α-BGT groups, and TNF-α and IL-6 contents were significantly increased in group DEX ( P<0. 05) . Compared with group II∕R, the W∕D ratio and contents of MDA, TNF-αand IL-6 were significantly decreased, SOD activity was increased (P<0. 05), and the pathological changes were significantly attenuated in group DEX. Compared with group DEX, the W∕D ratio and contents of MDA, TNF-α and IL-6 were significantly increased, SOD activity was decreased ( P<0. 05) , and the pathological changes were accentuated in group α-BGT. Conclusion Activation of cholinergic anti-inflammatory path-way is involved in the mechanism by which dexmedetomidine pretreatment reduces acute lung injury in a rat model of intestinal I∕R.
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Objective To evaluate the efficacy of different concentrations and small dose of lidocaine of combined spinal epi-dural anesthesia(CSEA) in elderly patients with non-procedure for prolapse and haemorrhoids(PPH) anorectal surgery .Methods One hundred and twenty elderly patients undergoing non-PPH anorectal surgery were selected and randomly dividedin to 4 groups , the group A(1 .5% lidocaine) ,B(1 .0% lidocaine) ,C(0 .8% lidocaine) and D ,30cases in each group .The group A ,B and C adopted CSEA ,and the group D adopted the sacral anesthesia .The changes of mean arterial pressure(MAP) and heart rate(HR) at different time points ,stress reactions before and after operation ,anesthetic operating time ,effect onset time ,postoperative reactivating time , anesthetic grade ,success rate ,postoperative patient satisfaction ,postoperative surgeon satisfaction and urine retention were recor-ded .Results MAP and HR at different time points had no statistical difference among 4 groups(P>0 .05) .The anesthetic onset time and postoperative activity recovery time in the group A ,B and C were significantly less than those in the group D(P<0 .01) . The postoperative activity recovery time in the group A was longer than that in the group B and C .The urine retention time in the group A ,B and C was significantly less than that in the group D (P<0 .05) .The postoperative patient satisfaction and surgeon sat-isfaction in the group A and B were 100% .Conclusion 1% lidocaine CSEA is more suitable for the elderly patients with non-PPH anorectal operation .
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BACKGROUND:Sufentanil exerts protective effects on tissues, but its roles in the repair of nervous system injury and the underlying mechanism are stil unknown. OBJECTIVE:To explore the protective effect of sufentanil preconditioning in the repair of spinal cord injuries and the underlying mechanism. METHODS:Mouse models of spinal cord injuries were prepared through clipping spinal cord fol owed by intraperitoneal injection of 3 and 6μg/kg sufentanil, respectively. RESULTS AND CONCLUISON:(1) Western blotting, ELISA and TUNEL assays showed that 6μg/kg sufentanil significantly down-regulated the protein expression levels of TLR4, nuclear factor-κBp65, cleaved-caspase 3, tumor necrosis factor-αand interlenkin-1βin the spinal cord of mice (P<0.05);at the same time, the number of apoptotic neurons was significantly decreased (P<0.05). (2) Furthermore, high-dose sufentanil preconditioning significantly ameliorated the recovery of limb function at 14 days after injury (P<0.05). (3) These results administrate that the neuroprotection provided by 6μg/kg sufentanil preconditioning for spinal cord injuries in mice maybe related to the TLR4/nuclear factor-κB signaling pathway inactivation.
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Objective To investigate the molecular mechanism how edaravone reduces cytotoxicity caused by hypoxia/reoxygenation-induced injury.Methods Ischemia model-hypoxia/ reoxygenation model which also called oxygen and glucose deprivation/reoxygenation model (OGD-R) was established.Cells were divided into control group,OGD-R group,OGD-R with edaravone of different concentration groups Cells of OGD-R model were pretreated with the appropriate concentration of edaravone or combine with the specific channel blockers LY294002 and MK2206 individually,the expression levels of ERK,AKT and Bcl-2 were detected with Western-blot,while the expression levels of BDNF and Bcl-2 mRNA detected with RT-PCR,the expression levels of BDNF protein detected with ELISIA,the levels of LDH releasing and Hoechst33258 staining used with homologue assay kit or regents.Results The pretreatment of cultured neurons with edaravone alleviated hypoxia/reoxygenation induced neuronal injury in a dose-dependent manner (LDH releasing reduced,Caspase-3 activity and ratio of nuclear pyknosis declined).The edaravone pretreatment did not increase significantly the p-ERK expression levels,but the amount of p AKT expression was significantly increased(P＜0.01).Pretreatment of edaravone(10 μmol/L) remarkably reduced the LDH release and declined the ratio of nuclear pyknosis after reoxygenation (P＜0.01),which was inhibited by MK2206.Compared to OGD-R,edaravone pretreatment markedly promoted BDNF and Bcl-2 mRNA expression at each time point,and the most pronounced effects occured at 8 h after OGDR.ELISIA analysis showed that BDNF protein level was significantly elevated after edaravone pretreatment at the same point.Western blot analysis indicted that edaravone pretreatment significantly enhanced Bcl-2 protein expression at 8 h after OGD-R,which was blocked by MK2206.Conclusions Edaravone may alleviate hypoxia/reoxygenation induced neuronal injury by enhancing BDNF and Bcl-2 expression and inhibiting Caspase-3 activity through activation of the PI3K/Akt pathway.