梗阻性黄疸对全麻术中丙泊酚用量的影响

目的探讨梗阻性黄疸对静脉麻醉中丙泊酚用量的影响。方法选择拟全身麻醉下行胆道或胰腺手术的患者35例,男24例,女11例,年龄35~70岁,ASAⅠ或Ⅱ级。根据术前1d的血清总胆红素(TBL)水平分为黄疸组(TBL17.1μmol/L,n=20)和对照组(TBL17.1μmol/L,n=15)。恒速输注丙泊酚0.3mg·kg~(-1)·min~(-1)进行麻醉诱导。输注开始后每隔20秒测试睫毛反射。记录两组患者至睫毛反射消失时丙泊酚用量,用多元线性回归(进入法)分析丙泊酚用量与血清TBL、总胆汁酸(TBA)、白蛋白(ALB)、天冬氨酸转移酶(AST)和丙氨酸转氨酶(ALT)之间的关系,用逐步法分析得出回归方程。结果至睫毛反射消失时黄疸组丙泊酚用量为(1.08±0.23)mg/kg,明显低于对照组的(1.38±0.24)mg/kg(P0.05)。黄疸组睫毛反射消失时丙泊酚用量与血清TBL存在明显的负性相关关系(r=-0.74,P0.05)。结论梗阻性黄疸患者在静脉麻醉中可减少丙泊酚用量。     

异氟醚吸入对老年大鼠长时程增强和脑源性神经营养因子的影响

目的通过观察异氟醚麻醉后老年大鼠海马长时程增强(LTP)和脑源性神经营养因子(BDNF)的变化,探讨术后认知功能障碍(POCD)的可能机制。方法健康雄性20月龄SD大鼠72只,随机分为异氟醚处理组(I组)和对照组(C组),每组36只。I组大鼠异氟醚吸入及维持浓度为1.2%,维持麻醉3h,以大鼠翻正反射的消失和恢复视为麻醉的开始和结束;C组大鼠不吸入麻醉药。I组大鼠分别于麻醉后7和14d断头,C组大鼠直接断头,常规切取海马组织,制备厚500μm的海马脑片,进行LTP斜率和幅值的测定,Western blot法检测BDNF表达水平。结果与C组比较,异氟醚处理后7和14dI组LTP的斜率和幅值均明显下降(P0.05)。与处理后7d比较,处理后14dI组LTP斜率和幅值均有明显升高(P0.05)。与C组比较,处理后7和14dI组BDNF表达水平明显下降(P0.05)。与处理后7d比较,处理后14dI组BDNF表达水平明显升高(P0.05)。结论异氟醚麻醉后,老年大鼠学习记忆能力损害可能持续14d以上,LTP的改变可能参与POCD的发生机制,并且与BDNF表达水平的降低有关。     

比较丙泊酚与七氟醚麻醉对梗阻性黄疸患者苏醒和术后恶心呕吐的影响

目的 比较丙泊酚靶控输注(TCI)与七氟醚吸入麻醉对梗阻性黄疽患者苏醒时间和术后恶心呕吐(PONV)的影响.方法 梗阻性黄疸患者60例,ASA Ⅰ或Ⅱ级,随机均分为丙泊酚组(P组)和七氟醚组(S组).术中均维持脑电双频指数(BIS)在40～55.记录患者麻醉前(T1)、气管插管后即刻(T2)、手术开始即刻(T3)及手术结束即刻(T4)的MAP、HR和BIS,记录停药后苏醒时间、苏醒时BIS和PONV发生率.结果 P组苏醒时间明显短于S组(P<0.05),苏醒时BIS明显低于S组(P<0.05).P组分别有3例和2例发生术后恶心和呕吐,S组分别有6例和4例(P<0.05).结论 在梗阻性黄疽患者丙泊酚TCI麻醉较七氟醚吸入麻醉PONV发生率较低,清醒较迅速.     

神经病理性疼痛大鼠FcγRⅠ mRNA表达量的变化

目的研究大鼠坐骨神经慢性压迫性损伤(chronic constriction injury of the sciatic nerve,CCI)发生后不同时期FcγRⅠmRNA表达量的变化。方法雄性Wistar大鼠72只随机分为三组:空白对照组(C组,n=8),假手术组(S组,n=32),CCI模型组(NP组,n=32)。C组不进行任何处理,S组只分离暴露坐骨神经后不结扎,NP组建立CCI模型。观察并记录术前和术后3、7、14和21d三组大鼠术侧后爪机械缩足阈值(mechanical withdrawal threshold,MWT)和右后爪热缩足潜伏期(thermal withdrawal latency,TWL)。RT-PCR检测术后3、7、14、21d时S组和NP组RTPCR脊髓、背根神经节的FcγRⅠmRNA表达。结果与术前比较,术后3、7、14和21dNP组MWT明显减少、TWL明显缩短(P0.05)。与NP组比较,术后3、7、14和21dC组、S组MWT明显增加、TWL明显延长(P0.05),术后3d的C组、术后3、7、14和21dS组脊髓和背根神经节的FcγRⅠmRNA表达明显减少(P0.05或P0.01)。结论坐骨神经慢性压迫性损伤大鼠脊髓海马和背根神经节FcγRⅠmRNA表达上调,可能与神经病理性疼痛的发生有关。     

柴胡皂苷d对阻塞性黄疸大鼠肝细胞游离钙及基质交联分子1的调控机制

目的 观察柴胡皂苷d(SSd)对阻塞性黄疸大鼠胆汁酸代谢、肝细胞游离钙及基质交联分子1(STIM1)基因表达的影响.方法 将108只SD雄性大鼠随机分为假手术对照组、阻黄组、阳性药物对照组、高、中、低剂量SSd组,同时各组随机分7、14、21d3个时段,每时段每组6只,建模成功后,分别连续给药7、14、21 d,于各时段末取肝组织和下腔静脉血标本,检测血清总胆汁酸(TBA);应用流式细胞仪通过荧光指示剂Fluo-3/AM测定肝细胞内钙离子浓度;逆转录-聚合酶链反应(RT-PCR)检测STIM1的mRNA表达.结果 阻黄模型建立7、14、21 d后,阻黄组血清TBA逐步增加,肝细胞游离钙平均荧光强度(MFI)值逐步上升,STIM1 mRNA表达逐步减弱;SSd治疗组7d末,与阻黄组比较,低、中、高剂量组TBA水平逐步下降,差异有统计学意义(P＜0.05);肝细胞游离钙MFI值逐步下调,差异有统计学意义(P＜0.05);STIM1 mRNA表达逐步增强,差异有统计学意义(P＜0.05);14、21 d末各检测指标变化趋势与7d末相同.结论 SSd能降低血清TBA浓度,上调STIM1 mRNA表达,抑制肝细胞钙超载,从而减轻阻塞性黄疸大鼠肝脏损害.     

丙泊酚后处理对大鼠蛛网膜下腔出血ET-1和iNOS的影响

目的 观察丙泊酚对大鼠蛛网膜下腔出血(SAH)继发性脑缺血缺氧性损害的作用效果以及作用机制.方法 将40只大鼠随机分为四组:造模后即刻丙泊酚后处理组(Ⅰ组)、造模后2h丙泊酚后处理组(Ⅱ组)、空白组(Ⅲ组)和出血对照组(Ⅳ组).分别在术前及术后7 d取血清测定内皮素-1(ET-1)浓度和诱导型一氧化氮合酶(iNOS)活力,并观察四组大鼠术后一般情况.结果 四组大鼠术前血清ET-1浓度和iNOS活力比较差异无统计学意义.Ⅰ、Ⅱ、Ⅳ组术后血清ET-1浓度和iNOS活力均高于术前(P＜0.05),其中Ⅰ、Ⅱ组术后均低于Ⅳ组(P＜0.05),而Ⅰ组又低于Ⅱ组(P＜0.05).结论 大鼠SAH后血清ET-1浓度和iNOS活力升高,丙泊酚可明显抑制其含量增加,早期应用丙泊酚对于降低血清ET-1浓度和iNOS活力的效果更为显著.     

大鼠梗阻性黄疸时肝细胞凋亡与肿瘤坏死因子的关系

目的：探讨梗阻性黄疸形成时肝细胞凋亡与肿瘤坏死因子的关系。方法：将72只Wistar大鼠随机分为正常组，假手术组和胆总管结扎手术组，以结扎胆总管（LCD）和Wistar大鼠为模型，采用放谢免疫法，测定血清中肿瘤坏死因子含量，末端脱氧核酸转移酶介导的末端标记法（TUNEL）检测在鼠肝细胞凋亡状态。结果：LCD术后3、7、14、21d肿瘤坏死因子含量明显高于正常组和假手术组，并于LCD术后7－14d达到高峰。LCD术后3、7、14、21d肝细胞凋亡指数（HAI）亦明显高于正常组和假手术组，且亦于7－14d达到高峰。的术组各时相肿瘤坏死因子与HAI呈正相关。结论：在Wistar大鼠梗阻性黄疸形成中肿瘤坏死因子对肝细胞凋亡起介导作用。     

精氨酸对恶性梗阻性黄疸患者肿瘤坏死因子-ɑ和可溶性白细胞介素2受体的影响

目的探讨精氨酸(Arginine,Arg)对恶性梗阻性黄疸患者围手术期肿瘤坏死因了浕(TNF-浕)和可溶性白细胞介素2受体(sIL-2R)的影响。方法选择经手术治疗的恶性梗阻性黄疸患者60例,随机分成常规治治疗组(R组)和加用精氨酸组(A组),每组30例。另取单纯性胆囊炎患者30例做对照组(C组)。R组术后给予常规营养支持,B组于术前1 d至术后7 d每日加用精氨酸20 g/d。分别于术前1 d、术后3 d、7 d、14 d取静脉血检测肝功能指标总胆红素(TB)、直接胆红素(DB)、丙氨酸氨基转移酶(ALT)、碱性磷酸酶(ALP)和TNF-浕及sIL-2R。结果A组病人术后7d及14d的肝功能TB、DB、ALT、ALP水平均较R组好转(P<0.01或P<0.05);A组病人TNF-浕和sIL-2R水平较R组明显下降,7 d时二组比较P<0.05,14 d时二组比较P<0.01。结论精氨酸能够减轻梗阻性黄疸对病人肝功能的损害,降低TNF-浕和sIL-2R的水平,改善梗阻性黄疸病人机体的免疫状态。     

黄芪对梗阻性黄疸大鼠肝功能的保护作用

目的:探讨黄芪注射液对实验性梗阻性黄疸大鼠肝功能的保护作用及作用机理.方法:SD大鼠行胆总管结扎后分别用3 mL黄芪注射液或生理盐水腹腔注射.术后测定血浆内皮素(ET-1)、血清超氧化物歧化酶(SOD)、丙二醛(MDA)含量,同时测定谷丙转氨酶(AST)、直接胆红素(DB)和总胆汁酸(TBA)浓度,并对肝脏行光镜下病理形态学观察.结果:血浆ET-1、血清MDA浓度在梗阻10 d即升高,随胆道梗阻时间延长进一步升高,SOD在梗阻10 d即下降,同时伴有血清AST、DB和TBA的升高和肝脏病理形态学的进行性改变.黄芪治疗组ET-1及MDA显著低于对照组,而SOD显著高于对照组,并能改善肝组织病理形态.结论:大鼠梗阻性黄疸时,血浆ET-1水平升高及氧自由基损害可能是肝损伤的原因,黄芪通过降低ET-1水平、抗氧化作用对梗阻性黄疸大鼠的肝脏起保护作用.     

丹参对梗阻性黄疸肾脏线粒体保护作用的实验研究

目的探讨氧自由基在梗阻性黄疸引发肾脏损害中的作用及丹参对肾脏线粒体的保护作用。方法将54只Wister大鼠随机分为假手术对照组(A组),胆总管结扎组(B组),胆总管结扎+丹参治疗组(C组)。采用胆总管结扎法(CBDL)建立大鼠梗阻性黄疸模型,C组应用丹参注射液5ml/(kg·d)腹腔注射治疗21d。3组大鼠分别于术后第7天(d7)、14天(d14)、21天(d21)处死,检测血清胆红素(BIL)、肌酐(Cr)、尿素氮(BUN)以及肾脏线粒体脂质过氧化产物丙二醛(MDA)和线粒体膜胆固醇含量的变化,观察肾脏及线粒体病理组织学改变,并作比较。结果B组及C组大鼠肾脏线粒体膜胆固醇及MDA含量高于对照组(P<0.05),但C组增高的程度低于B组(P<0.05),并且病理改变也较轻。结论氧自由基所引发的脂质过氧化作用是阻黄引起肾脏损害的重要原因之一,丹参可降低脂质过氧化作用对肾脏线粒体的损害作用,对梗阻性黄疸时的肾脏损害具有保护作用。     

缝隙连接在大鼠异丙酚和七氟醚麻醉中的作用

目的 评价缝隙连接在大鼠异丙酚和七氟醚麻醉中的作用.方法 雄性Wistar大鼠80只,体重210～260 g,采用随机数字表法,将大鼠随机分为8组(n=10):空白对照组(C组)、甘珀酸组(CA组)、异丙酚组(P组)、不同剂量甘珀酸+异丙酚组(CA1+P组、CA2+P组、CA3+P组)、七氟醚组(S组)、甘珀酸+七氟醚组(CA+S组).用立体定位仪定位大鼠侧脑室.C组侧脑室注射生理盐水2μl后腹腔注射生理盐水2ml,CA组侧脑室注射甘珀酸200μg后腹腔注射生理盐水2ml,P组、CA1+P组、CA2+P组和CA1+P组分别向侧脑室注射生理盐水2 μl、甘珀酸200、300和400μg后腹腔注射异丙酚5 mg/100 g,S组给予浓度梯度七氟醚,CA+S组侧脑室注射甘珀酸200μg后给予浓度梯度七氟醚,七氟醚初始浓度1%,梯度0.1%,记录翻正反射消失时间、翻正反射消失持续时间和翻正反射消失时七氟醚浓度.结果 C组与CA组大鼠均未出现翻正反射消失的麻醉作用;与P组比较,CA1+P组,CA2+P组,CA3+P组翻正反射消失时间缩短,翻正反射消失持续时间延长(P＜0.01);与CA+P组比较,CA2+P组,CA3+P组翻正反射消失时间缩短(P＜0.05);与S组比较,CA+S组翻正反射消失时七氟醚浓度减小(P＜0.05),翻正反射消失时间和消失持续时间差异无统计学意义(P＞0.05).结论 抑制缝隙连接功能虽然可强化异丙酚和七氟醚的麻醉作用,但不是其麻醉作用的主要机理.

Abstract：

Objective To evaluate the role of intercellular gap junction in the propofol and sevoflurane anesthesia in rats. Methods Eighty male Wistar rats weighing 210-260 g were randomly divided into 8 groups (n = 10 each): control group (group C), carbenoxolone group (group CA), propofol group (group P), different doses of carbenoxolone + propofol groups (groups CA1 + P, CA2 + P, CA3 + P), sevoflurane group (group S) and carbenoxolone + sevoflurane group (group CA + S). The animals ware anesthetized with intraperitoneal 10% chloraldurate 4 mg/kg and placed in a stereotactic apparatus to locate the lateral ventricle. In group C, after normal saline (NS) 2 μl was injected into the latersl ventricle, intraperitoneal NS 2 ml was injected. In group CA, after carbenoxolone 200 μg was injected into the lateral ventricle, intraperitoneal NS 2 ml was injected. In groups P,CA1 + P, CA2 + P and CA3 + P, NS 2 μl, and carbenoxolone 200, 300 and 400 μg were injected into the lateral ventricle respectively and then propofol 5 mg/100 g was injected intraperitoneally. Group S inhaled 1% sevoflurane (in increments of 0. 1% ) until the righting reflex was lost. Group CA + S inhaled 1% sevoflurane (in increments of 0.1% ) until the righting reflex was lost after carbenoxolono 200 μg was injected into the lateral ventricle. The time of loss of righting reflex, duration of loss of righting reflex and the sevoflurane concentration when the righting reflex disappeared were recorded. Results The loss of righting reflex did not appear in groups C and CA. Compared with group P, the time of loss of righting reflex was significantly shortened and duration of loss of righting reflex prolonged in groups CA1 + P, CA2 + P, CA3 + P ( P ＜ 0.01 ). The time of loss of righting reflex was significandy shorter in groups CA2 + P, CA3 + P than in group CA1 + P (P ＜ 0.05). The sevoflurane concentration when the righting reflex disappeared was significantly lower in group CA + S than in group S ( P ＜ 0.05 ). There was no significant difference in the time of loss of righting reflex and duration of loss of righting reflex between CA + S and S groups ( P ＞ 0.05). Conclusion Although inhibition of the function of gap junction can strengthen the anesthetic effects of propofol and sevoflurane, it is not the major mechanism.     

Inhibition of neuronal nitric oxide synthase reduces the propofol requirements in wild-type and nNOS knockout mice

BACKGROUND AND OBJECTIVE: The glutamate-nitric oxide-cyclic guanosine monophosphate pathway has been identified as a potential target for anaesthetic agents. However, mice deficient in neuronal nitric oxide synthase have a similar susceptibility to volatile anaesthetic agents to wild-type mice and are not affected by non-isoform selective inhibitors. We hypothesized that the neuronal nitric oxide synthase selective inhibitor, 7-nitroindazole, would also reduce the propofol requirements in wild-type mice but would have no effect in neuronal nitric oxide synthase knockout mice. METHODS: We determined the time to loss of righting reflex, time to painful stimulus and time to regaining the righting reflex in neuronal nitric oxide synthase knockout and wild-type mice following the intraperitoneal injection of propofol in untreated, 7-nitroindazole and vehicle only treated animals (n = 6 per group). Propofol (200 mg kg(-1)) resulted in loss of righting reflex in the untreated and vehicle only groups but was lethal in 7-nitroindazole pre-treated mice, requiring a reduced dose of propofol (100 mg kg(-1)). RESULTS: 7-nitroindazole pre-treatment significantly reduced the loss of righting reflex (P < 0.001) in both wild-type and knockout mice when compared to untreated and vehicle only pre-treated animals, but had no effect on time to painful stimulus or regaining of the righting reflex. 7-nitroindazole reduced the propofol requirements in knockout mice to the same extent as in wild-type animals. CONCLUSIONS: Propofol exerts its anaesthetic effects at least partially via the glutamate-nitric oxide-cyclic guanosine monophosphate pathway. The neuronal nitric oxide synthase knockout mice are sensitive to neuronal nitric oxide synthase selective inhibition suggesting that compensatory pathways in neuronal nitric oxide synthase knockout mice exist.     

柴芩四君子汤对胆囊切除术后患者粪胆汁酸代谢的影响

目的:探讨柴芩四君子汤对胆囊切除术后患者粪胆汁酸代谢的影响。方法:选取2017年10月—2019年9月在天津市南开医院诊断为胆囊结石并行胆囊切除术患者43例,采用随机数字表法分为胆囊切除术后对照组22例、柴芩四君子汤组21例,柴芩四君子汤组为胆囊切除术后第1天开始口服柴芩四君子汤,每天1剂,早晚分服,连服14 d。分别留取患者术前1 d、术后7 d和14 d粪便,采用液相色谱质谱法(LC-MS)测定胆酸(CA)、鹅脱氧胆酸(CDCA)、脱氧胆酸(DCA)、石胆酸(LCA)和熊去氧胆酸(UDCA)等5种粪胆汁酸含量,并计算初级胆汁酸(PBA)、次级胆汁酸(SBA)和总胆汁酸(TBA)含量。结果:与对照组比较,柴芩四君子汤组术前1 d粪CA、CDCA、DCA、LCA、UDCA、PBA、SBA和TBA含量差异均无统计学意义。术后14 d粪CA含量升高(P=0.007),CA/TBA、CDCA/TBA均升高(均P<0.05),DCA、LCA含量、DCA/TBA、LCA/TBA均降低(均P<0.05);PBA含量、PBA/TBA均升高(均P<0.05);SBA含量、SBA/TBA均降低(均P<0.05),TBA差异无统计学意义。结论:柴芩四君子汤可以调节CA、DCA、LCA、PBA、SBA含量及各胆汁酸相对含量。粪PBA含量增加以CA含量增加为特征。SBA含量降低以DCA、LCA含量降低为特征。     

升清胶囊对阻塞性黄疸患者微创术后细胞免疫功能的改善作用

目的 研究升清胶囊对阻塞性黄疸患者微创术后细胞免疫功能的改善作用.方法 将符合纳入标准的51例患者,采用简单随机方法分为研究组(升清胶囊组)、对照组(胆维他组)和空白组(常规治疗组),每组17例.术后空白组常规处理,不服用利胆药物;对照组除常规处理外,于术后第1天起口服胆维他;研究组除常规处理外,于术后第1天开始口服中药升清胶囊.术后第1、7天分别检测患者免疫指标CD3、CD4、sIL-2R、IL-10、TNF及TB.采用单因素方差分析的统计学方法对实验数据做统计处理.结果 研究组、对照组与空白组术后第1天CD3、CD4、sIL-2R、TNF、IL-10值比较均无统计学差异(P>0.05);术后第7天比较均有统计学差异(P<0.05).术后第7天CD.CD4、sIL-2R值与术后第1天比较,研究组比对照组均增高(P<0.05);时照组比空白组均增高(P<0.05);研究组比空白组均增高(P<0.05).术后第7天TNF值与术后第1天比较,研究组较对照组无显著性降低(P>0.05);对照组比空白组降低(P<0.05);研究组比空白组降低(P<0.05).术后第7天IL-10值与术后第1天比较,研究组比对照组降低(P<0.05);对照组比空白组无显著性降低(P>0.05);研究组比空白组降低(P<0.05).术后第1、7天各组间TB值比较均无统计学差异(P>0.05).结论 升清胶囊能更有效地加快阻塞性黄疸患者微创术后免疫功能的恢复,较不服用利胆药物及服用胆维他者有明显优势.     

低氧环境下异丙酚对新生大鼠学习记忆功能的影响

目的 探讨低氧环境下异丙酚对新生大鼠学习记忆功能的影响.方法 健康SD大鼠84只,日龄7 d,按照随机数字表法分为6组(n=14):异丙酚低氧组(PH组)、异丙酚空气组(PA组)和异丙酚纯氧组(PO组)分别腹腔注射异丙酚50 mg/kg,1次/d,连续7 d;生理盐水低氧组(CH组)、生理盐水空气组(CA组)和生理盐水纯氧组(CO组)腹腔注射生理盐水5.0 ml/kg,1次/d,连续7 d.每次注射完毕后分别放于低氧(18%O2)、空气和纯氧环境中.记录给药后SaO2和RR,待翻正反射恢复后放回鼠笼.于第7天注射完毕后24 h,各组随机取6只大鼠,取脑组织,观察海马神经元凋亡情况.其余大鼠于给药后2周进行Morris水迷宫实验,测试学习记忆功能.结果 与CO组比较,PO组RR降低,T1.2时逃逸潜伏期延长(P＜0.05);与CA组比较,PA组RR和SaO2降低,凋亡指数升高,逃逸潜伏期延长,穿越原平台区次数减少(P＜0.05);与CH组比较,PH组RR和Sa02降低,凋亡指数升高,逃逸潜伏期延长,穿越原平台区次数减少(P＜0.05);与PO组比较,PA组和PH组SaO2降低,凋亡指数升高,逃逸潜伏期延长,穿越原平台区次数减少(P＜0.05).CO组、CA组和CH组上述各指标差异无统计学意义(P＞0.05).结论 在低氧环境下,异丙酚可诱发新生大鼠海马神经元明显凋亡,降低学习记忆功能.     

L-精氨酸对大鼠阻塞性黄疸肝细胞线粒体内Ca2+的保护作用及其机制

目的 探讨L-精氨酸(L-Arg)对阻塞性黄疸大鼠肝细胞线粒体内Ca^2 保护作用及其机制。方法 将72只SD雄性大鼠随机分为对照组(SO组)，胆总管结扎 生理盐水组(BDL NS组)，胆总管结扎 L-Arg(BDL L-Arg组)。分别于术后7、14和21d检测肝细胞线粒体内MDA、SOD、Ca^2 含量。结果 BDL NS组各时间点肝细胞线粒体内Ca^2 、MDA含量明显升高，而SOD含量却明显降低。胆总管结扎7、14d时，肝细胞线粒体内Ca^2 、MDA含量BDL L-Arg组比BDL NS组低，差异有统计学意义(P＜0．01)；21d时，肝细胞线粒体内Ca^2 、MDA含量BDL NS组和BDL L-Arg中都更进一步升高，但两组比较差异无统计学意义(P＞0．05)。胆总管结扎7d时，肝细胞线粒体内SOD含量BDL L-Arg组比BDL NS组高(P＜0．05)；14、21d时，两组肝细胞线粒体内SOD含量都进一步下降，但差异无统计学意义(P＞0．05)。结论 L-Arg在阻塞性黄疸早、中期有保护线粒体作用，减少Ca^2 内流，不引起钙超载，减轻了阻黄时肝的损伤。     

MRI活体示踪PEG/PEI-SPIO标记脂肪源性干细胞移植治疗AD大鼠模型

目的 观察采用聚乙二醇/聚乙烯亚胺修饰超顺磁性氧化铁（PEG/PEI-SPIO）MRI活体示踪脂肪源性干细胞（ADSC）移植治疗阿尔茨海默病（AD）的可行性。方法 将48只AD模型大鼠随机均分为标记组、未标记组和磷酸缓冲盐溶液（PBS）组,分别向侧脑室内注入PEG/PEI-SPIO标记或未标记ADSC及PBS液;另取16只大鼠作为假手术组。分别于第7、14、21、28天行头部MRI,检测海马、颞顶叶皮质、小脑T2值及脑组织铁含量。结果 移植后各时间点标记组海马区及皮质区T2值均较其余3组缩短（P均<0.05）;第7、14天其皮质区T2值小于海马及小脑,第21、28天海马区T2值小于皮质及小脑（P均<0.05）。相同时间点标记组各脑区铁含量均较其余3组增加（P均<0.05）;移植第7、14天,标记组颞顶叶皮质区铁含量较海马及小脑增加（P均<0.05）,第21、28天海马区铁含量较颞顶叶皮质及小脑增加（P均<0.05）。结论 PEG/PEI-SPIO标记ADSC可反映其在AD模型鼠脑内的分布及迁移,并可通过MRI进行活体示踪。     

The effect of fibrin clot and C vitamin on the surgical treatment of Achilles tendon injury in the rat model✰

BackgroundThis study aimed to determine the histological, biochemical, and biomechanical efficacy of fibrin clot and vitamin C in the healing of Achilles tendon ruptures (ATR) in a rat model.Methods52 adult Wistar-Albino rats (300–450 g) were used in the study. 12 rats were divided into four groups as Monitor (Group I), Control (Group II), Fibrin Clot (Group III), Fibrin Clot with vitamin C (Group IV). Four rats were used for fibrin clot preparation. Fibroblast Growth Factor (FGF) and Vascular Endothelial Growth Factor (VEGF) were measured on the 3rd, 7th, 14th, and 21st days. Four rats were sacrificed on the 21st day from each group for histological evaluation. The rest of the rats were sacrificed at 42nd day, half for biomechanical and a half for histological evaluation.ResultsThe 42nd-day HSS score of group IV was significantly lower than those of group I, group II and group III (p = 0.036, p = 0.019, and p = 0.036, respectively). Group IV showed a significantly higher Maximum force N value than those of group I, group II and group III (p = 0.034, p = 0.034 and, p = 0.025, respectively). The blood FGF and VEGF levels of group III and group IV on the 3rd, 7th, 14th, and 21st days were higher than those of group I and group II (p < 0.05).ConclusionFibrin clot and vitamin C produced a stronger tendon structure in terms of biomechanics while providing histological and biochemically better quality tendon healing in the surgical treatment of ATR. This model can be used to accelerate high-quality tendon healing after ATR.Level of EvidenceLevel II, experimental study.     

The hypnotic and analgesic effects of 2-bromomelatonin

2-bromomelatonin is an analog of melatonin with a higher melatonin receptor affinity. We tested the hypnotic and analgesic properties of 2-bromomelatonin and compared them with those of propofol. Sprague-Dawley rats were assigned to receive 2-bromomelatonin or propofol IV, or morphine intraperitoneally. Righting reflex and response to tail clamping were assessed. Both 2-bromomelatonin and propofol caused a dose-dependent increase in the percent of rats displaying loss of both the righting reflex and the response to tail clamping. 2-Bromomelatonin was comparable to propofol in terms of its rapid onset and short duration of hypnosis. The 50% effective dose (95% confidence interval) for loss of righting reflex for propofol and 2-bromomelatonin were 3.7 (3.4-4.0) and 38 (35-41) mg/kg, respectively. Corresponding values for loss of response to tail clamp were 2.9 (3.5-4.0) and 21 (15-30) mg/kg, respectively. 2-bromomelatonin is approximately 6-10 times less potent than propofol depending on the end-point used. Intraperitoneal 30 mg/kg morphine did not affect the righting reflex, but resulted in loss of response to tail clamping in all animals. 2-bromomelatonin can exert hypnotic and antinocifensive effects similar to that observed with propofol. Unlike propofol, the reduced nocifensive behavior persisted after the animals had regained their righting reflex. This study provides evidence that 2-bromomelatonin has properties that are desirable in anesthetics or anesthetic adjuvants.