Objective To determine if the beneficial effects of transient desflurane application mitigates inflammation and decrease associated signaling induced by 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP) in mice. Methods Mice were induced to develop Parkinson’s disease (PD) by intraperitoneal injection with MPTP for 20 consecutive days, and validated mice were randomly allocated to four groups. Collected samples from euthanized mice were designated for the following analyses: 1) immunohistochemical staining for positive dopaminergic neurons in the substantia nigra and striatum, 2) immunofluorescence staining for ionized calcium binding adaptor molecule-1 (Iba1) and glial fibrillary acid protein (GFAP), and 3) western blotting for p38, p-p38, toll-like receptor 4, and tumor necrosis factor (TNF)-α. Results The inhalation of desflurane for 1 hour ameliorated locomotory dysfunctions of PD mice by recovering the loss of Iba1- and GFAP-positive dopaminergic neurons, deactivating microglial cells and astrocytes, and decreasing the amounts of inflammatory cytokines (TNF-α). Conclusions These findings suggest that transient desflurane inhalation may provide some benefits for PD through ameliorating inflammation and enhancing locomotor activity.

Posttraumatic stress disorder (PTSD) is a prevalent psychiatric disorder and sometimes deadly consequence of exposure to severe psychological trauma. However, there has been little known about the definitive molecular changes involved in determining vulnerability to PTSD. In the current study, we used proteomics to quantify protein changes in the hippocampus of foot shocks rats. A total of 6151 proteins were quantified and 97 proteins were significantly differentially expressed. The protein-protein interaction (PPI) analysis showed that oxidation-reduction process and glutathione homeostasis may be the potential key progress of being vulnerable to PTSD. The Gene Ontology analysis revealed enriched GO terms in the protein groups of Susceptible group vs Control group rats for glutathione binding,oligopeptide binding,modified amino acid binding,and glutathione transferase activity for their molecular functions (MF) and in the process of cellular response to toxic substance,xenobiotic metabolic process, urea metabolic process, and response to drug for the biological process (BP).SIGNIFICANCE:In recent years, there has been a growing interest in mental illness associated with trauma exposure. We found that stress susceptibility was associated with increased expression of arginase 1 indicated as a potential treatment target. Our results also proposed that carbonic anhydrases 3 could be a biomarker for the development of PTSD. This research helps to explain the potential molecular mechanism in PTSD and supply a new method for ameliorating PTSD.

背景:慢性病理性疼痛目前形成机制尚不明确,有研究认为脊髓损伤后CCL21可以激活中枢神经中的小胶质细胞,且仅在受损的神经元中表达,促进慢性病理性疼痛的形成.目的:探讨大鼠眶下神经结扎后,前扣带回皮质是否参与慢性病理性疼痛的形成,阻断前扣带回皮质中趋化因子CCL21是否可以减轻疼痛的发生.方法:雄性SD大鼠80只随机分成4组,每组20只.假手术组仅暴露大鼠眶下神经;模型组结扎大鼠左侧眶下神经;CCL21中和抗体组造模术后第7天于大鼠前扣带回皮质给予CCL21中和抗体;PBS组造模术后第7天于大鼠前扣带回皮质给予PBS溶液.假手术组及模型组大鼠分别于术后第3,5,7,14天开展行为学测试,CCL21中和抗体组及PBS组于给药后6 h进行行为学测试.所有大鼠行为学测试后麻醉处死,并取前扣带回皮质组织,采用Western Blot及免疫荧光法测定其中CCL21蛋白含量.结果与结论:①模型组大鼠术后痛阈较假手术组低,且前扣带回皮质中CCL21表达水平明显高于假手术组;②给予CCL21中和抗体之后,可看到CCL21表达有所降低,相对应大鼠痛阈也有相应的提升;③提示大鼠前扣带回皮质可能参与了慢性病理性疼痛的产生,且给予CCL21中和抗体可以改善疼痛.

Inhalation of anesthetic agents have been observed to confer neuroprotection for decades. The present study was intended to determine whether desflurane (DES) prohibits mast cells (MCs) from degranulation induced by lateral ventricular injection (LVC) with Compound 48/80 (C48/80) in C57BL/6. Total 100 mice were recruited to this study, but only 88 male mice (20–24 weeks) were survived from the procedure, and randomized and allocated into four groups: (A) the saline group; (B) the C48/80 group; (C) the sodium cromoglycate (CRO + C48/80) group; (D) 7.5% DES preconditioning for 2 h + C48/80 lateral ventricular injection (DES + C48/80) group. The slices of mice brain thalamus were performed for toluidine blue staining (MCs) and immunochemistry (fluorescence of Iba1 and GFAP, respectively), and brain tissues were extracted to probe IL-6, TNF-α, NF-κB (p65), and TLR4 against GAPDH by western blotting. Our results demonstrated that administration of C48/80 provoked degranulation of mast cells at thalamus, increasing the fluorescence intensities of Iba1 and GFAP, and over-expressing IL-6, TNF-α, NF-κB(p65), and TLR4. However, pre-conditioning inhalation of DES prohibited MCs from degranulation, diminishing the fluorescent intensities of Iba1 and GFAP, decreasing expressed levels of IL-6, TNF-α, NF-κB(p65), as well as TLR4. It suggests inhalation DES could inhibit the neuroinflammation and deactivate glial and astrocytes via direct prohibiting degranulation of MCs at thalamus in the central nervous system (CNS).

BACKGROUND:The pathogenesis of chemotherapy-induced neuropathy, a dose-dependent adverse effect of cisplatin, involves mitochondrial dysfunction. PTEN-induced putative kinase 1 (PINK1)/Parkin-mediated mitophagy removes damaged mitochondria under various pathological conditions. The objective of this study was to determine mitophagy status and its effects on mitochondrial function and neuronal cell damage after cisplatin treatment using an in vitro model of cisplatin-induced neurotoxicity. MATERIAL AND METHODS:PC12 cells were transfected with Parkin or Parkin siRNA using lentiviral particles and Lipofectamine 3000™, respectively, and then were exposed to 10 μM cisplatin. The expression of autophagic proteins was measured by Western blot analysis. Mitophagy in PC12 cells was detected by confocal microscopy analysis of mitochondria-lysosomes colocalization and autophagic flux. The effects of PINK1/Parkin-mediated mitophagy on cisplatin-induced neurotoxicity were assessed via mitochondrial function, neuritic length, nuclear diameter, and apoptosis. RESULTS:Cisplatin activated PINK1/Parkin-mediated mitophagy in PC12 cells. Autophagic flux analysis revealed that cisplatin inhibits the late stage of the autophagic process. The knockdown of Parkin suppressed cisplatin-induced mitophagy, aggravating cisplatin-induced depolarization of mitochondria, cellular ATP deficits, reactive oxygen species outburst, neuritic shortening, nuclear diameter reduction, and apoptosis, while Parkin overexpression enhanced mitophagy and reversed these effects. CONCLUSIONS:PINK1/Parkin-regulated mitophagy can protect against cisplatin-related neurotoxicity, suggesting therapeutic enhancement of mitophagy as a potential intervention for cisplatin-induced peripheral neuropathies. The interference of cisplatin with autophagosome-lysosome fusion may be partly responsible for cisplatin-induced neurotoxicity.

Multiple studies demonstrated that sepsis is a life-threatening state of organ dysfunction caused by infection and can induce neuroinflammation and cognitive impairment. The aim of this study was to evaluate the protective effects of attractylone (Atr) on sepsis-associated encephalopathy (SAE) and cognitive dysfunction. Moreover, we studied the underlying molecular mechanisms. We used an LPS-induced sepsis mouse model and evaluated the cognitive function with the Morris water maze and open field test. Neuronal damage in the hippocampus was assessed by immunohistochemical analysis. BV2 cells were used to identify the protective mechanism of Atr. The result showed that Atr attenuated LPS-induced cognitive impairment, neural apoptosis, inflammatory factors, and microglial activation. The in vitro experiment showed that Atr promoted silent information regulator 1 (SIRT1) expression and suppressed NFκB expression. Downregulation of SIRT1 reversed the protective effect of Atr in the LPS condition. Moreover, Atr-induced SIRT1 expression promoted BV2 from LPS-induced M1 to M2 phenotype. Taken together, these results indicated that Atr was a potential therapeutic agent for SAE and cognitive dysfunction.

Effects of NL1 on the expression level of neurexin-1β (Nrx1β) and the excitability of parvalbumin (PV) interneurons in mice with postoperative cognitive dysfunction (POCD) were explored. Eighty 10-month-old C57BL/6 male mice were randomly divided into four groups: control group, control+empty vector group (Control+EV), anesthesia surgery+empty vector group (POCD+EV group) and anesthesia+NL1 overexpression group (POCD+NL1 group), (n=20 per group). The behavioral differences of mice in the four groups were analyzed by means of open field test and fear conditioning test. The expression levels of NL1, PV and Nrx1β were detected by western blot analysis, and the binding between NL1 and Nrx1β was determined by co-immunoprecipitation. The expression level of postsynaptic density protein 95 (PSD95) in hippocampus and changes in the excitability of PV interneurons were further detected. Control and Control+EV groups had no significant difference in each index (P>0.05). Compared with Control+EV group, the percentage of cued freezing time in POCD+EV group decreased significantly, while percentage of cued freezing time was significantly increased in POCD+NL1 group and POCD+EV group (P<0.01). The differences in freezing time were not statistically significant among the 4 groups in the tone-related fear test (P>0.05). Then NL1 was overexpressed in mice with POCD, the protein levels of PV, Nrx1β and PSD95 were subsequently increased, and the interaction between NL1 and Nrx1β protein was enhanced, dramatically increasing the excitability of PV interneurons. The overexpression of NL1 can upregulate the expression levels of PV, Nrx1β and PSD95 in mice with POCD, enhance the interaction between NL1 and Nrx1β and further increase the excitability of PV interneurons, thus restoring the hippocampus-dependent memorial and cognitive impairment in POCD.

Emerging evidence showed that hyperpolarization-activated cation channels (HCN) participate in the development of inflammatory and neuropathic pain. However, the role of HCN2 in oxaliplatin-induced neuropathic pain remains unknown. Here, we found that HCN2 expression was upregulated in a rat model of oxaliplatin-induced neuropathic pain. Intrathecal injection of ZD7288, an HCN specific inhibitor, decreased the HCN2 level, as well as weakened the neuropathic pain behaviors compared to naive rats. Besides, mechanistic studies revealed that the expression of the spinal N-methyl-D-aspartate receptor subunit 2B was increased after oxaliplatin administration and was reduced by ZD7288 administration. The nociceptive behaviors were reversed by NR2B antagonist Ro 25-6981 in HCN2-overexpression rats. Furthermore, the underlying cellular mechanism demonstrated that ZD7288 administration restrained the enhanced activation of the neuronal calcium-calmodulin-dependent kinase II (CaMKII)/cyclic adenosine monophosphate response element-binding protein cascade after oxaliplatin administration. Moreover, pretreatment of CaMKII inhibitor KN-93 suppressed the nociceptive behaviors, as well as NR2B upregulation induced by overexpression of HCN2. In a word, HCN2 is conducive to oxaliplatin-induced neuropathic pain by activating the neuronal CaMKII/CREB cascade.

Background: During the last decade, total laparoscopic and laparoscopic-assisted distal gastrectomy for gastric cancer patients has been developed as alternatives to open resection. In recent years, this minimally invasive surgery has been extended using robotic-assisted surgery. Case presentation: Here, we report a surgical intervention using a Da Vinci surgical robot in which a lower two-third stomach resection with subsequent Billroth II gastrojejunostomy was performed. The patient was a 53-year-old male with complete situs inversus gastric cancer who had received 2 cycles of neo-adjuvant oxaliplatin combined with S-1 medication. The operation took 3 h in total without complications. The amount of bleeding was about 50 mL, and on day 5 after the operation, the patient was discharged. Conclusions: This is the first report of a successful robot-assisted gastric cancer resection of advanced gastric cancer in a patient with the anatomical abnormality of situs inversus totalis.

目的 比较内脏痛及炎性痛模型中羟考酮与吗啡的镇痛强度,并初步探讨羟考酮在内脏痛模型镇痛效应中μ、κ受体的比例.方法 SD大鼠360只.其中156只SD大鼠以腹腔注射2％醋酸4 mL/kg引起扭体反应作为内脏痛模型,随机均分为13组,分别为内脏痛对照组,羟考酮(0.4、0.64、1.0、1.6、2.6、4.2 mg/kg)组,吗啡(0.4、0.64、1.0、1.6、2.6、4.2 mg/kg)组;另将180只SD大鼠以左足底注射5％甲醛作为炎性痛模型,随机均分为15组,分别为炎性痛对照组,羟考酮(0.6、0.96、1.54、2.46、3.9、6.3、10.0 mg/kg)组,吗啡(0.6、0.96、1.54、2.46、3.9、6.3、10.0 mg/kg)组.通过行为药理学,分别计算羟考酮及吗啡的半数有效量(ED50).继续使用内脏痛模型,将24只SD大鼠随机均分为4组:对照组(D组)、羟考酮ED50组(E组)、κ受体拮抗剂Nor-BNI 20 mg/kg+羟考酮ED50组(K组)、μ受体拮抗剂naloxonazlne 20 mg/kg+羟考酮ED50组(U组),计算60 min扭体次数.结果 在内脏痛模型中,羟考酮ED50为0.6602 mg/kg(95％CI=0.02712～16.07 mg/kg)、吗啡为1.942 mg/kg(95％CI=0.2773～13.60 mg/kg),羟考酮ED50/吗啡ED50约为1:2.94;在炎性痛模型,I相羟考酮ED50为1.921 mg/kg(95％CI=1.199～3.077 mg/kg)、吗啡ED50为4.484 mg/kg(95％CI=1.797～11.19 mg/kg),比值约为1:2.334;Ⅱ相羟考酮ED50为2.262mg/kg(95％CI=1.378～3.715mg/kg)、吗啡ED50为3.812 mg/kg(95％CI=1.769～8.213mg/kg),比值约为1:1.69.在内脏痛模型中,D组扭体次数为(45.8±2.5)次,E组为(22.5±2.4)次,K组为(37.8±1.7)次,U组为(26.8±2.1)次,羟考酮发挥镇痛作用的κ、μ受体的比例约为2.375:1.结论 羟考酮ED50/吗啡ED50在甲醛炎性痛模型I相、Ⅱ相中的比值大于醋酸内脏痛模型,可能与羟考酮主要激动 κ 受体有关,且在2％醋酸扭体模型中羟考酮发挥镇痛效应的 κ、μ 受体的比例约为2.375:1.

枕大神经痛在疼痛诊疗中是一种常见病、多发病,在中医学中又称为"头痛"、"项痛". 该病的发病年龄较广,多数在 20 岁以上, 女性的发病率比男性略高,其主要临床表现是枕大神经分布区疼痛和感觉异常,主要症状为枕部和颅后部麻木、 疼痛以及头颈活动受限.

Objectives: To investigate the effects and possible mechanism of cobalt protoporphyrinⅨ(COPP), an inducible heme oxygenase agonist, on neuropathic pain (NP) by observing the alteration of expression and distribution of heme oxygenase-1 (HO-1) in the spinal cord of rats with sciatic nerve injury. Methods: Neuropathic pain was induced by the spared nerve injury (SNI). All male Sprague-Dawley rats were randomly assigned into 3 groups: Vehicle + Sham group, Vehicle + SNI group and COPP + SNI group. On the first day after operation, Vehicle (1%DMSO, 10 ml/kg) was intraperitoneally injected in Vehicle + Sham group and Vehicle + SNI group, and COPP (0.1%, 10 mg/kg) was intraperitoneally injected in COPP + SNI group. The paw withdrawal threshold (PWT) was measured before surgery and on day 3,7,14 after surgery. The expression of HO-1, μ-opioid receptor (MOR) andδ-opioid receptor (DOR) in the ipsilateral L4-6 lumbar segments of the spinal cord was analyzed by Western blotting on day 7 and 14 after surgery.Results:(1) At baseline, there was no significant difference of PWT among the three groups (P> 0.05). Compared with the&nbsp;Vehicle + Sham group, rats in the Vehicle + SNI group and SNI + COPP group showed significantly lower PWT from day 3 to 14 (P< 0.05). Compared with the Vehicle + SNI group, rats in the COPP+SNI group showed a significant improvement of PWT on day 7 and 14 after surgery (P< 0.05). (2) Compared with Vehicle+ Sham group, the expression of HO-1 in Vehicle+ SNI group was markedly increased (P< 0.05) on day 7 and 14;The expression of MOR and DOR were unaltered (P> 0.05); Compared with the Vehicle + SNI group, the expression of HO-1 and MOR increased significantly (P< 0.05) and DOR expression had no change (P> 0.05). Conclusion: Intraperitoneal injection of HO-1 agonist COPP reduced the mechanical allodynia of NP. The possible mechanism of these effects of COPP might be associated with the expression of opioid receptor.

Background: Intrathecal analgesia is more effective than conservative delivery methods such as drugs administered orally or intravenously. Programmable devices such as Medtronic’s SynchroMed systems have often been applied for long-term intrathecal analgesia. However, the totally implanted systems are very expensive in China. Considering cost-effectiveness, a reliable transmission protocol for a ZigBee-Based wireless analgesia pump system was used for long-term intrathecal analgesia in the home care of patients. Methods: We retrospectively investigated the efficacy, side effects, and complications of long-term intrathecal analgesia in the home care of patients via the wireless analgesia pump system. Follow-up visits occurred monthly for the initial 3 months after implantation and then every 3 months until patient death, withdrawal from the study, or removal of the device by a designated staff. At each follow-up visit, daily average pain score, pain frequency, satisfaction level, Spitzer Quality of Life Index, and side effects for every patient were recorded. Results: Pain intensity and frequency were significantly decreased by intrathecal analgesia via a wireless analgesia pump system. There were no significant differences in the satisfaction levels between hospitalization and each follow-up visit. The Spitzer Quality of Life Indexes were improved compared with patients who were hospitalized. No serious side effects were observed in this study. Conclusion: Intrathecal analgesia is an effective and safe method for control of refractory cancer pain, and wireless analgesia pump systems can be safely and effectively used for long-term intrathecal analgesia management in the home care of patients with advanced cancer.

Prenatal exposure to air pollution has been associated with autism spectrum disorder (ASD) risk but no study has examined associations with ASD severity or functioning. Cognitive ability, adaptive functioning, and ASD severity were assessed in 327 children with ASD from the Childhood Autism Risks from Genetics and the Environment study using the Mullen Scales of Early Learning (MSEL), the Vineland Adaptive Behavior Scales (VABS), and the Autism Diagnostic Observation Schedule calibrated severity score. Estimates of nitrogen dioxide (NO2), particulate matter (PM2.5 and PM10), ozone, and near-roadway air pollution were assigned to each trimester of pregnancy and first year of life. Increasing prenatal and first year NO2 exposures were associated with decreased MSEL and VABS scores. Increasing PM10 exposure in the third trimester was paradoxically associated with improved performance on the VABS. ASD severity was not associated with air pollution exposure.

Neuroinflammatory processes have a vital role in the pathogenesis of neuropathic pain. Garcinol, harvested from Garcinia indica, is known to exert potent anti-inflammatory properties. Recent studies have indicated that Garcinol may inhibit activation of nuclear factor-κB (NF-κB) by inhibiting NF-κB/p65 acetylation. These findings prompted us to evaluate the protective effects of Garcinol in the lumbar fifth spinal nerve ligation (SNL)-induced rat model of neuropathic pain and Lipopolysaccharide(LPS)-stimulated primary cultured microglia. In the present study, we found that intrathecal administration of Garcinol significantly attenuated SNL-induced nociceptive behaviors. Garcinol suppressed microglial activation as well as the expression of interleukin (IL)-1β, IL-6, inducible nitric oxide synthase (iNOS)/nitric oxide (NO), and cyclooxygenase-2 (COX-2)/prostaglandin E2 (PGE2) in the spinal cord of SNL rats. It also reduced the nuclear translocation of NF-κB by decreasing acetyl-p65 protein expression. Similarly, in the in vitro study, Garcinol decreased the production of NO/iNOS, PGE2/COX-2, and proinflammatory cytokines in LPS-exposed microglia. Likewise, Garcinol inhibited the NF-κB signaling pathway by downregulating acetyl-p65 levels in LPS-challenged microglia. Our findings suggest that Garcinol may have protective effects against neuropathic pain that are associated with the inhibition of neuroinflammation in microglia. Therefore, Garcinol could be a promising agent in the treatment of neuropathic pain.

Aim To investigate the effects of chemokine in the anterior cingulate cortex(ACC)of rats on the chronic neuropathic pain.Methods A model of trigeminal neuropathic pain was made by chronic constriction injury to the unilateral infraorbital nerve(CCI-ION).Eighty male Sprague-Dawley rats were randomly assigned into 4 groups(n=20): the sham group,the control group,the PBS treatment group and the anti-CX3CL1 treatment group.The unilateral infraorbital nerve was just exposed in the sham group; in the control group,the unilateral infraorbital nerve was exposed and ligated.The behavioral test was measured at 9 :00 am on day 1,3,5,7,14 after surgery separately.These rats were executed after behavioral tests,then tissues of ACC were removed to compare the protein expression levels of CX3CL1 and CD11b in two groups.The PBS solution and the CX3CL1 neutralizing antibody were injected into the ACC separately at 10 :00 am on the day with the highest level of CX3CL1 protein expression in the PBS treatment group and the anti-CX3CL1 treatment group.The behavioral test was measured 6 h later after the injection,and the tissue of ACC was removed to measure the protein expression levels of CX3CL1,CD11b and IL-1β of the two groups.Results At baseline,there was no significant difference in the feeling threshold among the four groups(P<005).Compared with the sham group,there was a significant reduction in the feeling threshold in the ipsilateral ION territory from 3 d to 14 d after CCI-ION in the control group(P<005).Rats given antibody in the anti-CX3CL1 treatment group showed an evident increase of the feeling threshold compared with the PBS group(P<005).Conclusion The ACC may take part in the chronic neuropathic pain via associating with the activated microglial cell and high-level of CX3CL1 expression.

目的 探讨姜黄素对海水吸入性肺损伤的防治作用及机制.方法 120只雄性SD大鼠随机均分为五组:空白对照组(C组)、生理盐水组(N组)、海水组(S组)、高剂量姜黄素100mg/kg组(CH组)、低剂量姜黄素20 mg/kg组(CL组).S组、CH组和CL组建立海水吸入模型.吸入海水前2d,姜黄素组每天腹腔注射姜黄素100或20mg/kg,2次/天,C、N和S组腹腔注射等容PBS溶液.测定吸入海水前(基础值,T1)、吸入海水后15 min(T2)、30 min(T3)、1 h(T4)、4 h(T5)、24 h(T6)时PaO2、PaCO2、右肺中叶湿干重比(W/D).T3时测定左肺下叶丙二醛(MDA)和超氧化物歧化酶(SOD)的浓度,右肺下叶组织行常规病理切片检查.结果 T2时N组,T2～T4时S、CH和CL组PaO2明显低于C组(P＜0.05);T2～T4时S、CH和CL组PaCO2明显高于C组(P＜0.05).T2～T4时N组PaO2明显高于,PaCO2明显低于S组(P＜0.01).T2、T3时CH组PaO2明显高于S组(P＜0.05).S、CH和CL组MDA明显高于C组(P＜0.05);N组和CH组MDA明显低于,SOD明显高于S组(P＜0.05).T2～T4时S、CH和CL组肺组织W/D明显高于C组(P＜0.05);T2～T4时CH组和N组肺组织W/D明显低于S组(P＜0.05).海水吸入后S组出现明显的肺泡破裂,肺泡、肺间质水肿,炎细胞浸润,CH组能明显减轻肺组织损伤及炎性细胞浸润,但CL组与S组差异无统计学意义.结论 预防性使用姜黄素100 mg/kg能减轻海水(4 ml/kg)吸入导致的早期(1h内)肺损伤,其机制可能与其减轻肺组织的氧化应激有关.

(1.Department of Anesthesiology, Jinling Hospital, School of Medicine, Nanjing University, Nanjing 210002, Jiang-su, China;2.Department of Anesthesiology, General Hospital of Shenyang Military Region, PLA, Shenyang 110000, China) <br> le-blind, 60 patients scheduled for OPCABG were randomly divided into 4 groups: control group( group C) and 3 dexmedetomidine group(group D1、D2、D2).Patients in each group received saline or dexmedetomidine 0.2μg/kg, 0.4μg/kg, 0.6μg/kg respectively. Hemodynamic variables such as HR、MAP、CVP、MPAP、PCWP、SVRI and PVRI were recorded after entering into the operationroom ( T0 ) , before the anesthesia induction( T1 ) , at 5 minutes after tracheal intubation ( T2 ) , during the sternotomy( T3 ) , at the end of an-astomosis of left anterior descending(T4), at the end of anastomosis of right coronary artery or 1eft circum flex coronary artery(T5) and after operation ( T6 ) .Body tempreture and urine volume were recorded during the operation.Total quantity of analgesics consumption and heart adverse reaction( bradyarrhythmia, tachycardia, hypotension, hypertension etc) were also recorded. Results At T2 -T6 , there was a significant decline in HR, MAP, SVRI, PVRI and CI in group D2 and group D3 compared with group C (P<0.05).SVRI and PVRI in group C and group D2 significantly increased at T3 -T6 compared with those at at T0(P<0.05).At T2 and T6, HR and MAP in group group D2 signicantly increased compared with group D3([57 ±6]times/min vs [52 ±4] times/min, [72 ±7]mmHg vs [63 ±5]mmHg;[72 ±5]times/min vs [55 ±6]times/min, [68 ±5]mmHg vs [63 ±5]mmHg)].At T4 -T6, significant difference was found in CI, SVRI and PVRI between group D2and group D3(P<0.05).In comparison to group C, hypertension, tachycardia in-cidence, noradrenaline amount and isosorbide mononitrate amount declined significant in group D2and group D3(P<0.05);hypoten-sion and bradycardia incidence increased significantly while isosorbide mononitrate amount reduced significantly(P <0.05). Conclusion In OPCABG, dexmedetomidine infused at 0.4μg/(kg· h) after a loading dose of 0.5μg/(kg· 10 min) is useful in maintaining stable hemodynamics which contributes to oxygen balance and reduces myocardium injury in patients.

Seawater drowning-induced acute lung injury (ALI) is a serious clinical condition characterized by increased alveolar-capillary permeability, excessive inflammatory responses, and refractory hypoxemia. However, current therapeutic options are largely supportive; thus, it is of great interest to search for alternative agents to treat seawater aspiration-induced ALI. Erythropoietin (EPO) is a multifunctional agent with antiinflammatory, antioxidative, and antiapoptotic properties. However, the effects of EPO on seawater aspiration-induced ALI remain unclear. In the present study, male rats were randomly assigned to the naive group, normal saline group, seawater group, or seawater + EPO group. EPO was administered intraperitoneally at 48 and 24 h before seawater aspiration. Arterial blood gas analysis was performed with a gas analyzer at baseline, 30 min, 1 h, 4 h, and 24 h after seawater aspiration, respectively. Histological scores, computed tomography scan, nuclear factor kappa B p65, inducible nitric oxide synthase, caspase-3, tumor necrosis factor-alpha, interleukin (IL)-1β, IL-6, IL-10, wet-to-dry weight ratio, myeloperoxidase activity, malondialdehyde, and superoxide dismutase in the lung were determined 30 min after seawater aspiration. Our results showed that EPO pretreatment alleviated seawater aspiration-induced ALI, as indicated by increased arterial partial oxygen tension and decreased lung histological scores. Furthermore, EPO pretreatment attenuated seawater aspiration-induced increase in the expressions of pulmonary nuclear factor kappa B p65, inducible nitric oxide synthase, caspase-3, tumor necrosis factor-alpha, IL-1β, myeloperoxidase activity, and malondialdehyde when compared with the seawater group. Collectively, our study suggested that EPO pretreatment attenuates seawater aspiration-induced ALI by down-regulation of pulmonary pro-inflammatory cytokines, oxidative stress, and apoptosis.

Aim: Seawater drowning induced-acute lung injury (ALI) is a serious clinical condition characterized by refractory hypoxemia, enhanced alveolar-capillary permeability, hemorrhage, and uncontrolled overwhelming inflammatory responses. Hydrogen sulfide (H2S) is an endogenous gaseous mediator that plays an important role in the physiological and pathophysiological conditions, especially in some inflammatory diseases. However, the beneficial effects of sodium hydrosulfide (NaHS), a H2S donor, on seawater aspiration-induced ALI remains to be elucidated. Material and methods: Two hundred and forty rats were equally assigned to the naive group, normal saline group, seawater group, or seawater + NaHS group. NaHS or vehicle was intraperitoneally administered immediately after seawater aspiration. Arterial blood gas analysis was performed with a gas analyzer at baseline, 30 min, 1 h, 4 h, and 24 h after the seawater aspiration, respectively. Histological scores, computed tomography scan, TUNE-positive cells assay, Toll-like receptor 4, nuclear factor kappa B p65, caspase-3, tumor necrosis factor-alpha, interleukin (IL)-1 beta, IL-6, IL-10, wet-to-dry weight ratio, myeloperoxidase activity, malondialdehyde, and superoxide dismutase levels in the lung were assessed at 30 min after the seawater aspiration. Results: NaHS treatment alleviated ALI as demonstrated by the increased arterial partial oxygen tension and deceased lung histological scores, which was accompanied by decreased TUNEL-positive cells, Toll-like receptor 4, nuclear factor kappa B p65, caspase-3, tumor necrosis factor-alpha, IL-1 beta, myeloperoxidase activity, and malondialdehyde in the lung. Conclusions: Our study suggested that the protective effects of NaHS on seawater aspiration-induced ALI might be associated with its anti-inflammatory, anti-oxidative, and anti-apoptotic properties.