Sigma-1受体在小鼠肝缺血再灌注损伤中的表达和作用

目的 研究Sigma-1受体在小鼠肝缺血再灌注损伤中的表达和作用。方法 将20只小鼠随机分为对照组和肝缺血再灌注组,建立小鼠肝缺血再灌注模型。肝缺血再灌注组分别为缺血1 h再灌注6 h、再灌注12 h和再灌注24 h组。实时荧光定量PCR及Western Blot实验分别检测各组小鼠肝组织Sigma-1受体mRNA及蛋白表达水平。进一步研究Sigma-1受体在小鼠肝缺血再灌注损伤中的作用,将20只小鼠随机分为对照组、缺血再灌注组、Sigma-1受体激动剂组、Sigma-1受体激动剂加抑制剂组。建立小鼠肝缺血再灌注模型1 h前,向激动剂组小鼠腹腔注射Sigma-1受体激动剂4-苯基-1-(4-苯丁基)哌啶,激动剂加抑制剂组小鼠腹腔注射激动剂4-苯基-1-(4-苯丁基)哌啶和抑制剂NE-100。再灌注12 h后通过实时荧光定量PCR检测肝组织肿瘤坏死因子-α（tumor necrosis factor-α,TNF-α）、白介素（interleukin,IL）-6和IL-10 mRNA表达水平,ELISA法检测血清TNF-α、IL-6和IL-10水平,检测血清谷丙转氨酶（alanine aminotransferase,ALT）及谷草转氨酶（aspartate aminotransferase,AST）,苏木精-尹红染色法观察肝组织病理学变化。结果 同对照组比较,缺血1 h再灌注12 h组Sigma-1受体表达水平明显升高(P<0.05)。同肝缺血再灌注组比较,Sigma-1受体激动剂组小鼠肝组织TNF-α和IL-6 mRNA表达水平下降,IL-10 mRNA表达水平升高,血清TNF-α、IL-6水平降低,IL-10水平升高,血清ALT、AST水平降低,肝组织病理学损伤减轻(P<0.05)。Sigma-1受体激动剂加抑制剂组小鼠肝组织TNF-α和IL-6 mRNA表达水平较Sigma-1受体激动剂组升高,IL-10 mRNA表达水平下降。血清TNF-α、IL-6水平升高,IL-10水平降低,血清ALT、AST水平升高,肝组织病理学损伤加重(P<0.05)。结论 在小鼠肝缺血再灌注后,Sigma-1受体表达水平升高,促进Sigma-1受体活化可减轻肝缺血再灌注损伤,其机制可能与抑制炎症反应有关。     

谷氨酰胺对入肝血流阻断后肠道损伤的影响及机制探讨

目的探讨谷氨酰胺（Gln）对入肝血流阻断后肠道损伤的影响及其机制。方法将雄性Wistar大鼠120只,随机分为3组：假手术组（1组）、对照组（2组）和实验组（3组）。每组40只。2组和3组采用Pringle＇s法进行入肝血流阻断,持续35分钟,在阻断前3组大鼠腹腔注射Gln（300mg／kg,用生理盐水稀释至4ml）,每天2次,连续5天。每组随机抽取10只大鼠分别于阻断前及再灌注后2、4、24小时,测定肠组织丙二醛（MDA）含量,检测血清肿瘤坏死因子-α（TNF-α）及门静脉内毒素水平。光镜观察并测定肠黏膜厚度、肠绒毛高度。采用逆转录聚合酶链反应（RT—PCR）法检测再灌注后24小时肠道高迁移率族蛋白B1（HMGB1）mRNA的表达。结果与1组相比,再灌注后2、3组MDA含量、TNF-α及内毒素水平增高（P〈0．05）,而肠黏膜厚度、肠绒毛高度下降（P〈0．05）。与2组相比,再灌注后3组MDA含量、TNF-α及内毒素水平降低（P〈0．05）,而肠黏膜厚度、肠绒毛高度明显增加（P〈0．05）。再灌注后24小时,与2组相比,1、3组HMGB1mRNA表达水平均明显降低（P〈0．05）。结论Gln能够抑制人肝血流阻断后内毒素移位、炎性因子释放及肠道HMGB1mRNA的表达,具有减轻肠道损伤的作用。     

谷氨酰胺预处理对肝缺血-再灌注后肺损伤的干预效果及机制

目的观察谷氨酰胺预处理对肝缺血-再灌注后急性肺损伤的干预效果。方法成年SD雄性大鼠36只,按随机数字表法将其平均分为三组:假手术组(Sham,S组);缺血-再灌注组(I-R组);谷氨酰胺组(Gln,G组)。其中I-R组为完全阻断肝动脉、门静脉及胆总管(参照Pringle's法)持续缺血30 min后再灌注1 h;而G组以0.75 mg/kg谷氨酰胺于全肝血流阻断前60 min经尾静脉注射行预处理。测定肺组织肿瘤坏死因子-α(TNF-α)、核因子-κb(NF-κb)、髓过氧化物酶(MPO)活性;肺湿/干重比(W/D);HE染色观察肺组织形态学变化以及谷氨酰胺预处理对大鼠肝缺血-再灌注后肺组织热休克蛋白-70(HSP-70)表达的影响。结果与I-R组比较,G组大鼠肺组织W/D比、TNF-α、NF-κb水平明显下降,MPO活性显著降低,HSP-70蛋白表达水平明显增加(P<0.05),光镜下肺组织损伤明显改善。结论谷氨酰胺预处理可通过增加肺组织HSP-70表达,抑制NF-κb等炎症因子的释放,对肝脏缺血-再灌注后的急性肺损伤起到一定的保护作用。     

常温下大鼠肝缺血再灌注损伤的实验研究

目的 探讨大鼠肝脏缺血再灌注损伤的机制。方法 采取大鼠第一肝门阻断的缺血再灌注模型,将健康雄性SD大鼠32只随机分为4组：A组（假手术组）、B组（肝缺血40分钟组）、C组（肝缺血40分钟再灌注2小时组）和D组（肝缺血40分钟再灌注4小时组）,观察每组动物的病理切片,分别检测血浆谷丙转氨酶（ALT）、乳酸脱氢酶（LDH）、肿瘤坏死因子-α（TNF-α）以及肝组织匀浆中的丙二醛（MDA）和内皮素-1（ET-1）的含量,免疫组化测定P-选择素的表达。结果 肝脏缺血再灌注后,B、C、D组血浆肝功能酶学指标显著升高,随着再灌注时间的延长升高更为明显（C、D组与B、A组比较及D组与C组比较,P〈0．01）;C、D组血清TNF-α活性升高,以再灌注2小时最明显（C组与A、B组比P〈0．01）;C、D组肝组织中MDA活性升高,以再灌注2小时最明显（C组与A、B组比P〈0．01）;C、D组肝组织中ET-1活性升高,以再灌注4小时最明显（D组与A、B、C组比P〈0．01）;C、D组肝组织中P-选择素表达增加,以再灌注2、4小时最明显（C、D组与A、B组比P〈0．01）;光镜下表现再灌注4小时肝组织明显水肿变性,部分有片状坏死,肝窦淤血并变窄。结论 大鼠肝脏微循环障碍是肝脏缺血再灌注损伤的病理基础,枯否氏细胞产生的细胞因子和氧自由基在中性粒细胞的激活过程中起主要调节作用,肝脏对内皮素等缩血管物质的调节紊乱也是微循环产生障碍的重要因素。     

丙泊酚对兔肝脏缺血后再灌注损伤的保护作用

目的探讨丙泊酚对兔肝脏缺血后再灌注损伤的影响。方法将实验兔随机分为拟手术组(S组),肝脏缺血后再灌注组(IR组),及微量泵连续静脉输注丙泊酚[10mg/(kg.h)]组(PRO组),IR组和PRO组将入肝血流阻断25min后再灌注120min,然后观察不同时相丙氨酸氨基转氨酶(ALT)、天冬氨酸氨基转氨酶(AST)、乳酸脱氢酶(LDH)的变化,检测肝组织超氧化物歧化酶(SOD)活性及丙二醛(MDA)含量。结果IR组、PRO组再灌注120min后肝功能均有损害,而IR组的ALT,AST,LDH均高于PRO组;PRO组肝脏组织MDA浓度低于IR组(P<0.05),PRO组的SOD浓度高于IR组(P<0.05)。结论肝脏缺血后再灌注可使大量氧自由基释放,它在肝损伤中发挥重要作用,丙泊酚可抑制再灌注后的过度氧化反应,减轻肝组织损伤。     

右美托咪啶对大鼠肝缺血再灌注损伤的保护作用

目的探讨右美托咪啶对大鼠急性肝缺血再灌注损伤（ischemiareperfusioninjury,IRI）的保护作用。方法sD大鼠32只,随机分为对照组（S组）、缺血-再灌注组（IR组）、右美托咪啶组（Dex组）、右美托咪啶＋育亨宾组（Dex＋Yoh组）,每组8只。IR组制备大鼠肝缺血再灌注模型。Dex组通过尾静脉以5μg／（kg·h）的速度持续泵注右美托咪啶1h,余同IR组。Dex＋Yoh组静脉输注右美托咪啶前10min,静脉注射育亨宾1mg／kg,其余同Dex组。分别测定血清AST、ALT活性,肿瘤坏死因子-α（TNF-α、自细胞介素-6（IL-6）浓度,肝组织超氧化物歧化酶（SOD）活性、丙二醛（MDA）含量,光镜观察肝组织的病理学变化。结果与S组比较,IR组血AST、ALT、TN-α、IL-6,肝组织MDA水平显著增加,SOD水平下降（P〈0．05）;与IR组比较,Dex组血AST、ALT、TNF-α、IL-6下降（P〈0．05）,肝组织SOD水平升高,MDA水平下降（P〈0．05）,Dex＋Yoh组无显著变化（P〉0．05）;形态学上,病理损伤程度与生化指标相符合。结论右美托咪啶能减轻肝缺血再灌注损伤,其机制可能是激活d,肾上腺素受体,抑制氧自由基反应和炎性因子的释放。     

还原型谷胱甘肽对肝缺血再灌注损伤核因子-κB影响的实验研究

 目的探讨核因子-κB在肝缺血再灌注损伤中的表达和还原型谷胱甘肽的保护作用.方法将90只健康家兔随机分为对照组、肝缺血再灌注组和还原型谷胱甘肽保护组,制备肝缺血再灌注损伤模型.观察三组肝组织中核因子-κB的表达、血清ALT、丙二醛(MDA)及血浆TNF-α含量和肝脏的病理变化.结果正常肝组织中仅偶见肝细胞核因子-κB的表达,肝缺血再灌注损伤时,核因子-κB的表达明显增强,ALT、MDA、TNF-α含量显著升高(P＜0.01),肝脏出现坏死,大量炎性细胞浸润;使用还原型谷胱甘肽后,上述指标的异常变化均明显减轻,其差异有显著性意义(P＜0.01或P＜0.05).结论核因子-κB参与了肝缺血再灌注损伤,还原型谷胱甘肽能抑制其表达,对肝缺血再灌注损伤有积极的保护作用.     

甘氨酸对大鼠创伤性休克继发肝损伤的防护作用

目的 研究甘氨酸对大鼠创伤性休克后肝组织热休克蛋白70(HSP70)和TNF-αmRNA表达的影响,探讨其对大鼠创伤性休克继发肝损伤的可能保护机制.方法 建立创伤性休克动物模型,120只Wistar大鼠按随机数字表法分成3组:创伤性休克组(休克组)、甘氨酸治疗组(治疗组)和对照组.在复苏开始时,治疗组大鼠将甘氨酸按100 mg/kg溶于0.5 ml等渗盐水后经颈静脉输入,休克组输以同体积的等渗盐水.分别于复苏后3,6,12,24及48 h 5个时相点处死大鼠.采用RT-PCR法检测肝组织HSP70和TNF-α mRNA表达;观察肝组织病理改变并测定血清ALT和AST水平. 结果 休克组复苏后3 h肝组织HSPTO和TNF-αmRNA表达即增加,复苏后6 h达高峰,治疗组肝组织HSP70 mRNA表达于复苏后12 h达高峰.与休克组比较,治疗组各时相点肝组织TNF-α mRNA表达明显降低(P<0.05),HSP70 mRNA表达明显增强(P<0.05),血清ALT和AST明显降低(P<0.05),肝组织光镜下病理损害明显改善(P<0.05). 结论甘氨酸可能通过增强肝组织HSP70 mRNA表达及抑制TNF-α mRNA表达的途径降低创伤性休克后继发肝损伤的程度.     

糖原合成酶激酶-3β抑制剂对肝热缺血再灌注损伤的保护

目的：研究糖原合成酶激酶-3β（GSK-3β）抑制剂TDZD-8对大鼠肝脏热缺血再灌注损伤的保护作用。方法：将大鼠随机分为4组：A组（假手术＋空白对照）、B组（假手术＋TDZD-8）、C组（I／R＋空白对照）和D组（I／R＋TDZD-8,实验组）。通过肝门阻断30min建立大鼠缺血再灌注模型,分别于再灌注后2、12h,每组各选取8只大鼠,测定血清ALT、AST含量,行肝组织形态学检测;TUNEL检测肝细胞凋亡,计算凋亡指数（AI）;采用实时定量PCR方法检测肝Bcl-2mRNA转录水平。结果：预先给予TDZD-8组在缺血再灌注期各时相点肝组织结构受损相应较轻,血清ALT、AST含量及凋亡指数均较低（P〈0．05）;Bcl-2mRNA则显著上升。结论：GSK-3β抑制剂可显著减轻肝脏缺血再灌注损伤程度,上调肝脏Bcl-2mRNA转录,抑制肝细胞凋亡。     

大鼠肝缺血再灌注后急性肺损伤的实验研究

为探讨肝缺血再灌注致急性肺损伤的发病机制 ,采用大鼠部分肝缺血再灌注模型 ,将健康雄性SD大鼠 2 4只随机分为 3组(每组均为 8只 ) :A组 (手术对照组) ,B组 (肝缺血 90min组 ) ,C组 (肝缺血 90min再灌注 12 0min组 )。分别测定血浆中天冬氨酸转氨酶(AST)、丙氨酸转氨酶 (ALT)、乳酸脱氢酶 (LDH)、肿瘤坏死因子 (TNF α)、白介素 1β(IL 1β)和支气管肺泡灌洗液中总蛋白以及肺组织干湿重比的变化 ;观察光镜下肺组织病理变化及各组血压的动态变化。结果显示 :①缺血再灌注各组与对照组比较 ,血浆中ALT、AST、LDH浓度明显升高 ;②肺干湿重比值明显降低 ,支气管肺泡灌洗液中总蛋白含量显著升高 ;③C组血浆TNF α、IL 1β分别为 (1 2 7± 0 6 2 )ng/ml、(0 2 2±0 5 3)ng/ml,与A组比较明显升高(P <0 0 5 ) ;④肝缺血期血压没有明显降低 ,再灌注发生后血压开始下降 ,最低血压与对照组比较有明显差异 (P <0 0 1) ,约 30min后血压回升到正常 ;⑤缺血再灌注后有明显肺泡内和肺间质水肿及炎症细胞浸润。提示肝缺血再灌注后释放细胞因子TNF α、IL 1β可致急性肺损伤     

星状神经节阻滞对大鼠严重创伤后垂体-甲状腺、肾上腺皮质轴的影响

目的 观察大鼠严重创伤后垂体-甲状腺、肾上腺皮质轴变化及星状神经节阻滞(SGB)的影响.方法 建立大鼠严重创伤(右侧胸部撞击伤复合同侧股骨闭合性骨折)模型,动物分3组:正常对照组(n=12);创伤治疗组(n=12),创伤后即刻、8小时以0.125%布比卡因0.3ml行SGB;创伤对照组(n=12),于同一部位给予0.3ml生理盐水.于创伤后24小时取动脉血,测定血浆促肾上腺皮质激素(ACTH)、皮质醇(GC)、促甲状腺激素(TSH)、三碘甲状腺原氨酸(T3)、甲状腺素(T4)水平.结果 创伤后血浆T3、T4水平较正常对照组降低(P<0.05),但TSH变化不显著,行SGB后TSH、T3、T4尽管数值上增加,但变化不明显;创伤后血浆ACTH、GC水平较正常对照组升高(P<0.01、P<0.05),行SGB后ACTH、GC水平降低(P<0.01、P<0.05).结论 严重创伤后垂体.甲状腺、肾上腺皮质轴发生明显变化,SGB能减轻其变化.     

受者同系骨髓间充质干细胞对心脏移植大鼠的免疫调节作用

目的 观察静脉注射受者同系骨髓间充质干细胞(MSC)对大鼠心脏移植免疫反应的影响.方法 以20只成年雄性Lewis大鼠作为心脏供体,20只成年雄性Wistar大鼠作为受体,将其随机分为2组,每组10只,行颈部心脏移植:对照组(A组)手术后24h,经尾静脉注射3ml 0.9％氯化钠注射液;MSC处理组(B组)手术后24h,经尾静脉注射2×106个MSC(悬浮于3ml 0.9％氯化钠注射液中).术后1周,每组随机取受体大鼠4只,检测静脉血及移植物CD4+、CD8+、CD4+CD25high、CD4+CD25highfoxp3+T细胞占总淋巴细胞的比例,计算CD4+/CD8+比值.其余6只大鼠用于继续观察移植物存活时间.结果 A组大鼠移植心脏存活7.2±1.3d,B组大鼠移植心脏存活14.8±2.9d,两组间差异有统计学意义(P＜0.01).B组静脉血中CD4+/CD8+值、CD4+CD25highT细胞占总淋巴细胞的比例、CD4+CD25highFoxp3+T细胞占总淋巴细胞的比例(分别为1.18±0.07、2.51％±0.56％、2.05％±0.62％)均明显高于A组(分别为0.49±0.05、0.96％±0.19％、0.82％±0.09％),差异有统计学意义(P＜0.01).移植心脏中CD4+/CD8+值在两组间无统计学差异(P＞0.05);B组移植心脏中CD4+CD25highT细胞及CD4+CD25highFoxp3+T细胞占总淋巴细胞的比例(分别为2.74％±0.28％、2.54％±0.31％)均明显高于A组(分别为0.61％±0.06％、0.53％±0.06％),差异有统计学意义(P＜0.01).结论 静脉注射受者同系骨髓MSC可诱导大鼠心脏移植免疫耐受,延长移植心脏的存活时间.     

Effects of radiographic contrast media on pulmonary vascular resistance of normoxic and chronically hypoxic pulmonary hypertensive rats.

Intravascular radiographic contrast media (RCM) can be associated with significant morbidity in patients with pulmonary hypertension (PH). This study investigated the direct effect of the four main classes of RCM (high osmolar ionic monomer "diatrizoate"; low osmolar ionic dimer "ioxaglate"; low osmolar non-ionic monomer "iopromide"; and iso-osmolar non-ionic dimer "iotrolan") in ex vivo isolated rat lungs perfused with blood at 20 ml min(-1) under basal conditions (air + 5% CO2 ventilation, pulmonary artery pressure (Ppa) 16-20 mmHg) and when Ppa was raised by hypoxic vasoconstriction in normal rats (2-3% O2+5% CO2 ventilation, Ppa increased by 4-14 mmHg). The effects of low osmolar RCM (ioxaglate, iopromide and iotrolan) were also studied in rats with PH induced by chronic hypoxia (3 weeks 10% O2, Ppa 26-36 mmHg). Increasing volumes (0.05 ml, 0.1 ml, 0.3 ml, and 0.5 ml) of RCM, mannitol (osmolar and pH control) or normal saline (volume control) were added to the 10 ml blood reservoir (n=4-9 per group). In normal rats, RCM caused a dose-dependent slow rise in Ppa. The maximum rise in mean+/-SEM Ppa at the cumulative dose of 0.95 ml was ioxaglate 13.8+/-1.6 mmHg>iotrolan 7.3+/-1.7 mmHg=diatrizoate 9.8+/-2.2 mmHg>iopromide 3.0+/-0.8 mmHg (p<0.05). The rise in Ppa induced by ioxaglate and iotrolan was significantly greater than in the mannitol and saline controls (p<0.05). Pre-treatment with endothelin receptor A/B blockade (SB209670) did not abolish the rise in Ppa induced by diatrizoate (0.95 ml) in the normal rat (3.8+/-1.3 mmHg diatrizoate alone and 3.4+/-1.1 mmHg in the presence of 40 microM SB209670, n=5 per group). When Ppa was raised by acute hypoxia, ioxaglate and diatrizoate (0.5 ml) caused a fall in Ppa (percentage fall -53+/-23 and -118+/-10, respectively, p<0.001) while iotrolan and iopromide caused a small further rise in Ppa, which was significant with iotrolan at a dose of 0.3 ml (percentage rise in pressure 14.2+/-2.3, p<0.05). In chronic pulmonary hypertensive rats, RCM (0.95 ml) caused an overall slow progressive rise in Ppa (iopromide 6.8+/-1.7 mmHg< ioxaglate 11.6+/-2.5 mmHg=iotrolan 12.7+/-1.1 mmHg). However, ioxaglate initially induced an acute fall of Ppa (maximum fall 4.22+/-0.9 mmHg, p<0.05) for almost 20 min. In summary, iopromide induced the least change in Ppa of normal and pulmonary hypertensive rats. The pathophysiology of the effects of RCM on the pulmonary circulation remains uncertain.     

多黏菌素B干预颅脑创伤后大鼠外周血LPS表达的变化

 目的 探讨多黏菌素B(PMB)干预颅脑创伤后大鼠外周血肠道细菌崩解产物脂多糖(LPS)表达的变化。方法 选取健康7周龄成年雄性SD大鼠50只,随机分为5组,正常组(Normal)、假手术组(Sham)、创伤性脑损伤组(TBI)、创伤性脑损+生理盐水组(TBI+ NS组)及创伤性脑损+多黏菌素组(TBI+PMB组),每组10只。通过电子皮质损伤撞击仪(eCCI)造模, 分别计算Normal、Sham、TBI组大鼠造模前后24、48 h神经功能缺损评分(NSS)。造模后48 h,这三组大鼠给予FD4灌胃,检测循环中FD4的浓度间接反映肠道通透性改变;TBI+PMB组使用1 ml注射器经腹腔注射PMB溶液(2.5 μg/ml),TBI+ NS组给予等体积生理盐水。记录实验前,试验第1、3、5、7 天 共5个时间点的(试剂终点显色法检测)外周血中LPS的浓度;并结合7 d脑组织(石蜡包埋HE染色)炎症评分评估脑组织炎症反应。结果 与Sham组比较, Normal组外周血中FD4的浓度升高[(2743±279)ng/ml vs. (1850±80) ng/ml)],TBI组外周血中FD4的浓度明显增高[(4228±203)ng/ml vs. (2743±279)ng/ml],LPS浓度在第3天时显著升高,差异均有统计学意义(P<0.05)。其余时间点差异无统计学意义。与TBI+NS组比较,TBI+PMB组LPS浓度在术后第3天明显降低[(0.56±0.04)EU/ml vs.(0.94±0.03)EU/ml];炎症评分TBI组和TBI+NS组明显下降,差异均有统计学意义(P<0.05)。结论 大鼠急性TBI后可出现肠道菌群移位及外周血LPS水平一过性增加,PMB能降低TBI后早期LPS浓度,减少急性TBI后脑组织炎症反应。     

富氢液对脓毒血症大鼠肠黏膜屏障保护作用及机制研究

目的探讨富氢液对脓毒血症大鼠肠黏膜屏障的影响及其可能机制。方法清洁级SD大鼠30只,随机分为假手术组(sham组)、脓毒血症组(SEP组)及富氢液处理组(C组),每组10只。sham组仅开腹,显露盲肠;C组和SEP组行盲肠结扎穿孔术,再分别静脉给予富氢液和等量生理盐水。3组大鼠均于模型建立4 h后处死,观察小肠组织病理学结果;酶联免疫吸附法(ELISA)检测肠脂肪酸结合蛋白(I-FABP)、D-乳酸、肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)、白细胞介素-10(IL-10)浓度;蛋白质印迹(Western-blot)法检测B淋巴细胞瘤-2基因(Bcl-2)、Bax、Caspase-3蛋白表达水平。结果光镜下sham组未出现病理损伤,SEP组损伤较重,C组损伤较轻。与sham组比较,SEP组I-FABP、D-乳酸升高[(817.12±50.39)ng/ml比(378.54±40.50)ng/ml;(513.84±42.91)ng/ml比(329.98±38.11)ng/ml,P<0.05]。与SEP组比较,C组I-FABP、D-乳酸降低[(548.92±42.19)ng/ml比(817.12±50.39)ng/ml;(437.89±36.12)ng/ml比(513.84±42.91)ng/ml,P<0.05]。与sham组比较,SEP组TNF-α、IL-6、IL-10升高[(196.51±30.31)ng/ml比(75.54±10.21)ng/ml;(68.69±3.39)ng/ml比(20.97±2.38)ng/ml;(149.61±20.21)ng/ml比(80.69±13.51)ng/ml,P<0.05];与SEP组比较,C组TNF-α、IL-6降低,IL-10升高[(118.47±10.14)ng/ml比(196.51±30.31)ng/ml;(45.36±5.14)ng/ml比(68.69±3.39)ng/ml;(178.52±26.31)ng/ml比(149.61±20.21)ng/ml,P<0.05]。与sham组比较,SEP组Bcl-2蛋白表达升高,Bax与Caspase-3降低(P<0.05);与SEP组比较,C组Bcl-2蛋白表达降低,Bax与Caspase-3升高(P<0.05)。结论富氢液对脓毒血症大鼠肠黏膜屏障有保护作用,其机制与抑制凋亡相关因子有关。     

Effects of oxytocin on high intensity focused ultrasound (HIFU) ablation of adenomysis: A prospective study

Objective

To investigate the effects of oxytocin on high-intensity focused ultrasound (HIFU) ablation for the treatment of adenomyosis.

Materials and methods

Eighty-six patients with adenomyosis from three hospitals were randomly assigned to the oxytocin group or control group for HIFU treatment. During HIFU treatment, 80 units of oxytocin was added in 500 ml of 0.9% normal saline running at the rate of 2 ml/min (0.32 U/min) in the oxytocin group, while 0.9% normal saline was used in the control group. Both patients and HIFU operators were blinded to oxytocin or saline application. Treatment results, adverse effects were compared.

Results

When using oxytocin, the non-perfused volume (NPV) ratio was 80.7 ± 11.6%, the energy-efficiency factor (EEF) was 8.1 ± 9.9 J/mm³, and the sonication time required to ablate 1 cm³ was 30.0 ± 36.0 s/cm³. When not using oxytocin, the non-perfused volume ratio was 70.8 ± 16.7%, the EEF was 15.8 ± 19.6 J/mm³, and the sonication time required to ablate 1 cm³ was 58.2 ± 72.7 S/cm³. Significant difference in the NPV ratio, EEF, and the sonication time required to ablate 1 cm³ between the two groups was observed. No oxytocin related adverse effects occurred.

Conclusion

Oxytocin could significantly decrease the energy for ablating adenomyosis with HIFU, safely enhance the treatment efficiency.     

伏立诺他对严重烫伤大鼠心脏的保护作用

 目的 研究伏立诺他(SAHA)对严重烫伤大鼠心脏的保护作用及机制。方法 雄性SD大鼠48只,随机分为假烫组、烫伤组和SAHA组,每组16只,烫伤组和SAHA组采用沸水水浴法制作50％TBSA Ⅲ度烫伤动物模型,伤后即刻腹腔内分别注射0.25 ml生理盐水或SAHA(7.5 mg/kg,溶于0.25 ml生理盐水),假烫组以37 ℃水浴代替沸水。每组根据烫伤后3、6 h两个观察时间点,又分为两个亚组,每亚组8只大鼠,分别于烫伤后3 h和6 h两个时间点取大鼠腹主动脉血,测定血浆肌酸激酶同工酶(CK-MB)水平,然后处死动物取心肌组织,干/湿重法测定心肌组织含水率,TUNEL方法检测心肌凋亡细胞率,caspase-3活性试剂盒测定心肌组织内caspase-3活性。结果 烫伤后3、6 h,烫伤组血浆内CK-MB[(2552.9±145.3)U/L,(5418.7±292.9)U/L]水平较假烫组[(585.6±46.1)U/L]明显升高,心肌组织含水率[(77.65±1.75)%,(80.23±1.82)%]较假烫组[(70.12±1.99)%]明显升高,心肌细胞凋亡率[(16.1±0.8)%,(21.5±1.2)%]较假烫组[(0.5±0.1)%]明显升高、caspase-3活性[(0.716±0.052)μmol/mg,(0.912±0.063)μmol/mg]较假烫组[(0.435±0.041)μmol/mg]明显升高,差异均具有统计学意义(均P＜0.05);而给予SAHA处理后,CK-MB水平[(1642.4±157.2)U/L,(3475.3±187.5)U/L]、心肌组织含水率[(72.31±1.95)%,(75.21±2.00)%]、心肌细胞凋亡率[(11.6±0.6)%,(15.1±0.9)%]、caspase-3活性[(0.557±0.052)μmol/mg,(0.535±0.034)μmol/mg]较烫伤组明显下降,差异均有统计学意义(均P＜0.05)。结论 在严重烫伤大鼠治疗中,SAHA能显著降低血浆内CK-MB水平及心肌组织含水率,保护心脏功能,可能与减少心肌细胞凋亡、降低心肌组织内caspase-3活性有关。     

Multi-detector row CT of the head and neck: comparison of different volumes of contrast material with and without a saline chaser

Introduction The aim of this study was to determine the effect of different volumes of contrast material with and without a saline chaser on tissue enhancement in multidetector row CT (MDCT) of the head and neck.Methods In a blind prospective fashion, 120 patients were randomized into the following four groups: group 1, 80 ml contrast material administered at a flow rate of 2.0 ml/s; group 2, 80 ml followed by 40 ml saline at 2.0 ml/s; group 3, 60 ml at 1.5 ml/s; and group 4, 60 ml followed by 30 ml saline at 1.5 ml/s. The attenuation values of the carotid artery, internal jugular vein, and muscle were measured at an interval of 1.5 s in each patient. The degree of perivenous artifacts was subjectively assessed.Results Mean attenuation values in the carotid artery and internal jugular vein were significantly higher in groups 1 and 2 than in groups 3 and 4. The width of the diagnostic window (both carotid and jugular enhancement >150 HU) were significantly longer in groups 1 and 2 than in groups 3 and 4. The addition of a saline chaser did not result in improved vascular enhancement or a wider diagnostic window, but reduced perivenous artifacts, compared with using contrast material alone.Conclusion Reduction of contrast material from 80 to 60 ml results in insufficient enhancement of neck vessels. In addition, the benefit of a saline chaser technique is not obvious except for its ability to reduce perivenous artifacts.     

Inhibition of tryptophan hydroxylase abolishes fatigue induced by central tryptophan in exercising rats

Fatigue during prolonged exercise is related to brain monoamines concentrations, but the mechanisms underlying this relationship have not been fully elucidated. We investigated the effects of increased central tryptophan (TRP) availability on physical performance and thermoregulation in running rats that were pretreated with parachlorophenylalanine (p‐CPA), an inhibitor of the conversion of TRP to serotonin. On the 3 days before the experiment, adult male Wistar rats were treated with intraperitoneal (ip) injections of saline or p‐CPA. On the day of the experiment, animals received intracerebroventricular (icv) injections of either saline or TRP (20.3 μM) and underwent a submaximal exercise test until fatigue. Icv TRP‐treated rats that received ip saline presented higher heat storage rate and a 69% reduction in time to fatigue compared with the control animals. Pretreatment with ip p‐CPA blocked the effects of TRP on thermoregulation and performance. Moreover, ip p‐CPA administration accelerated cutaneous heat dissipation when compared with saline‐pretreated rats. We conclude that an elevated availability of central TRP interferes with fatigue mechanisms of exercising rats. This response is modulated by serotonergic pathways, because TRP effects were blocked in the presence of p‐CPA. Our data also support that a depletion of brain serotonin facilitates heat loss mechanisms during exercise.