目的 探讨罕见血管活性肠肽瘤(VIPoma)患者手术治疗的围术期麻醉管理.方法 回顾性总结2019年11月11日至24日厦门大学附属翔安医院收治,主诉持续腹泻6年,诊断为神经内分泌肿瘤,择期开腹行腹膜后肿瘤切除术+射频消融术1例患者的围术期麻醉管理经验.结果 术中实施了全身麻醉复合咽喉部表面麻醉及双侧腹横肌平面阻滞.综合麻醉管理包括:术前进行奥曲肽治疗;完善补钾、纠酸、抑制血管活性肠肽(VIP)等术前准备;术中监测有创血压,动态监测血气分析;着重维持血流动力学稳定、水电解质平衡、保护重要脏器功能等.手术顺利完成,患者腹泻症状消失,电解质水平恢复正常且稳定,好转出院.结论 VIPoma围术期麻醉管理较为复杂、风险较高,但抓住该肿瘤患者术前基础及术中易发生血液动力学波动等特点,做好麻醉预案,选择合适的麻醉方式,并精心综合管理,有利于保证手术成功.

The role and mechanism of ketamine in anesthesia have been widely studied and reported. Recent studies have found that ketamine is closely associated with inflammation, which can be used as a regulator of inflammatory response and stress-induced immune disorder and takes a positive or negative regulatory role in the pathogenesis of inflammation-related diseases. The current review focuses on the anti-inflammatory and pro-inflammatory effects and mechanisms of ketamine in sepsis and inflammatory diseases, so as to provide new targets, methods and strategies for the use of ketamine in medical practice.

目的 研究丙泊酚复合舒芬太尼靶控输注对上腹部开腹手术患者苏醒质量的影响.方法 选取2019年4月至2020年4月于厦门大学附属翔安医院择期行上腹部开腹手术的60例患者为研究对象,采用随机数字表法分为对照组和研究组,每组30例.二组患者均采用丙泊酚复合舒芬太尼靶控输注,靶浓度分别为3μg/ml和0.35ng/ml,丙泊酚诱导时记录患者意识消失时效应室浓度,术中全凭静脉麻醉.对照组术毕前10min停止丙泊酚及舒芬太尼输注;研究组关腹时将丙泊酚靶控输注浓度降至意识消失时的效应室浓度维持至手术结束、舒芬太尼浓度降至0.25ng/ml直至患者清醒拔管.观察两组患者在各时间点的平均动脉压和心率,以及拔管时间及定向力恢复时间.结果 两组患者均无术中知晓,研究组血流动力学较对照组更稳定,拔管时间以及定向力恢复时间研究组较对照组均明显缩短,差异均有显著性(P<0.05).结论 关腹时采用丙泊酚(浓度为意识消失时的效应室浓度)复合舒芬太尼靶控输注(浓度为0.25ng/ml)的用药方案,患者无术中知晓,术毕苏醒快,安全性高,可用于上腹部开腹手术麻醉.

[Objective] To compare the effects of different analgesic methods on pain and early rehabilitation after total knee arthroplasty (TKA).[Methods] From September 2016 to September 2017,75 patients who would undergo unilateral total knee arthroplasty were enrolled in this study.In term of postoperative analgesia,the patients were randomly divided into three groups,including the continuous adductor canal block combined with periarticular local infiltration analgesia (the CA + P group),continuous femoral nerve block combined with periarticular local infiltration analgesia (the CF+P group) and continu ous epidural analgesia group (the E group).All patients received TKA under combined spinal and epidural anesthesia.The VAS,quadriceps muscle strength,maximum active flexion angle and adverse reactions were compared among the three groups.[Results] At 24,48 and 72 hours postoperatively,the moving VAS of the E group was statistically higher than the CA+P group and the CF+P group (P＜0.05).The strength of quadriceps femoris of the CF+P group and E group statistically decreased at 6,12 and 24 hours (P＜0.05).The flexion angle of knee joint was significantly decreased in CF+P group and E group at 1,2 and 3 days (P＜0.05).The additional intravenous analgesic drug dosage and postoperative complication in the E group were significantly higher than the other two groups (P＜0.05).[Conclusion] Continuous adductor canal block combined with periarticular local infiltration analgesia does effectively relieve pain in patients with total knee arthroplasty,with minimized impact on quadriceps muscle strength and less adverse reactions.

Objective: The effect of Aβ1-42 induced microglia inflammatory response on the expression of methylated CpG binding protein (Mecp2) in hippocampal neurons in vitro. Methods: (1) The treatment of microglia cell line (N9) with different concentrations of Aβ1-42 (final concentration of 0, 5, 10, 20, 30 μmol/L), 24 h after the supernatant, ELISA detection of each N9 cell culture supernatant in inflammatory factor TNF-α, IL-1β, the choice of Aβ1-42 concentration. (2) The treatment of microglia cell line (N9) with Aβ1-42 (final concentration of 20 μmol/L) and TLR4 antagonist TAK-242 (final concentration of 1 μg/ml). It was divided into 3 groups: normal control group (group con), simple Aβ1-42 treatment group (group Aβ1-42 ) and TAK-242 intervention group after Aβ1-42 treatment (group TAK-242). After 24 h, the supernatant was taken, and the content of the inflammatory factors TNF-α and IL-1β in the culture supernatant of N9 cells in each group was detected by ELISA. (3) The experimental grouping is the same as (2), the culture fluid was collected after 24 h to interfere with the well grown hippocampal neuronal cell line (HT-22). After 24 h, the expression of Mecp2 protein in each HT-22 cell was detected by Western Blot and immunofluorescence staining. Results: (1) The results of ELISA showed that compared with the con group, after Aβ1-42 treatment, the expression of TNF-α and IL-1β secreted by N9 cells increased with the increase of Aβ1-42 concentration (P＜0.05). (2) The results of ELISA showed that compared with the con group, the expression level of TNF-α and IL-1β in Aβ1-42 group was significantly increased (P＜0.05); The level of TNF-α and IL-1β secreted in the TAK-242 group were significantly lower than those in the Aβ1-42 group (P＜0.05). (3) The results of Western Blot showed that compared with the con group, the expression of Mecp2 protein in the Aβ1-42 group HT-22 cells increased significantly (P＜0.05). Compared with the Aβ1-42 group, the Mecp2 protein expression in the HT-22 cells of the TAK-242 group decreased significantly (P＜0.05). (4) Immunofluorescence staining showed that compared with the con group, the expression of Mecp2 protein in the HT-22 cells increased significantly in the Aβ1-42 group, while the expression of Mecp2 protein in the HT-22 cells of the TAK-242 group was weaker than that of the Aβ1-42 group. Conclusion: Aβ induced inflammatory reaction in micro-glia can lead to neuronal damage, probably due to the increased expression of Mecp2 protein in neurons and the damage of neurons.

目的:探讨配对免疫球蛋白样受体B(paired immunoglobulin-like receptor B,PirB)在神经元氧糖剥夺(oxygen and glucose deprivation,OGD)后加重神经元损伤及其可能的分子机制.方法:培养SD原代大鼠皮层神经元,利用pirb RNAi慢病毒载体干扰PirB RNA表达,进行OGD 1 h,OGD后24h进行Western Blot分别检测Bcl2和Bax蛋白的表达情况,并检测线粒体和胞浆Cyt c的含量;应用透射电镜观察神经元的超微结构改变.结果:OGD后神经元内Bcl2的表达明显下调,Bax表达却显著上调(P＜0.05).但是OGD +pirb RNAi组Bcl2的表达明显增加,而Bax的表达显著减少(P＜0.05).OGD后24 h,Cyt c从线粒体漏出显著增加,而OGD+ pirb RNAi组Cyt c漏出显著减少(P＜0.05).透射电镜结果显示:OGD后神经元呈现不同程度的细胞核固缩现象,线粒体明显肿大、嵴断裂、基粒减少.而OGD +pirb RNAi组神经元的这些超微结构改变显著减轻.结论:PirB可能通过调节Bcl2和Bax的表达,影响线粒体Cytc的释放,加重神经元损伤,siRNA能显著抑制PirB表达,对OGD后神经元的损伤具有保护作用.

Objective:To study the effect of mild hypothermia treatment on miR-199a expression in the ischemic penumbra after MCAO and on the neuroprotection.Methods:Adult male Sprague-Dawley rats were used.The middle cerebral arterial occlusion (MCAO) model was established.At 30 min after reperfusion,the head of rats treated with mild hypothermia for 3 h.At 6 h,24 h and 72 h after reperfusion,the expression of miR-199a was tested in the penumbra.At 24 h after reperfusion,the brain water content and neurological deficit scores (NDS) were evaluated.At 24 h after reperfusion,the NISSL and FJC staining in the penumbra was measured.Results:(1) Compared with the MCAO group at 24 h after reperfusion,the expression of miR-199a was decreased in MCAO group at 6 h and 72 h after reperfusion (P ＜0.05).At 6 h,24 h and 72 h after reperfusion,compared with every Sham group,the expression of miR-199a was increased in every MCAO group (P ＜ 0.05);Compared with every MCAO group,the expression of miR-199a was decreased in every MCAO + MHT group (P ＜ 0.05).(2) At 24 h after reperfusion,compared with MCAO + MHT group,the NDS was higher (P ＜ 0.05),the water content was more (P ＜ 0.05),the density of normal neurons in the ischemic penumbra was decreased (P ＜ 0.05) and the number of FJC-positive neurons was less (P ＜ 0.05) in MCAO group and in MCAO + MHT + miR-199a mimics group.Conclusion:Mild hypothermia treatment attenuated brain damage and enhanced neural function recovery by alleviating neuronal damage and degeneration through inhibiting miR-199a expression in the ischemic penumbra after cerebral ischemia injury.