硫化氢在脓毒症大鼠心肌损伤中的作用

目的 研究硫化氢(H2S)在脓毒症大鼠心肌损伤中的作用.方法 雄性SD大鼠60只,月龄3～4个月,体质量180 ～220 g,随机(随机数字法)分为4组:对照组(Ⅰ组)、脓毒症组(Ⅱ组)、脓毒症+ NaHS(H2S供体)预处理组(Ⅲ组)、脓毒症+PAG(H2S代谢酶CSE抑制剂)组(Ⅳ组),每组各15只.采用盲肠结扎穿孔法制作脓毒症大鼠模型,观察各组大鼠血流动力学改变,测定心肌组织中H2S的变化,采用RT-PCR方法观察CSE mRNA表达,采用髓过氧化物酶(MPO)测定试剂盒测定各组心肌组织MPO含量,用ELISA方法检测心肌组织TNF-α、IL-1β的表达,光学显微镜下观察心肌形态学改变.结果 与Ⅰ组相比,Ⅱ组血压下降,心肌组织中H2S、TNF-α、IL-1β、MPO含量出现不同程度增加(P＜0.01或P＜0.05),CSE mRNA表达水平提高(P＜0.05);与Ⅱ组相比,Ⅲ组血压下降更为显著,心肌组织中H2S、TNF-α、IL-1β含量增加,MPO活性增强(P＜0.05),但CSE mRNA表达水平并无显著改变;与Ⅱ组相比,Ⅳ组血压水平接近,心肌组织中H2S、TNF-α、IL-1β 含量均降低,MPO活性减弱(P＜0.05),CSE mRNA表达水平下降(P＜0.05).四组心肌组织形态学损伤由轻到重依次为Ⅰ、Ⅳ、Ⅱ、Ⅲ.结论 脓毒症大鼠心肌组织CSE/H2S体系上调,给予H2S可以升高脓毒症大鼠心肌组织中MPO、TNF-α、IL-1β水平,加重心肌损伤,给予H2S抑制剂可以减轻心肌损伤.     

饱和氢气盐水对大鼠急性肺损伤的保护作用

目的 探讨饱和氢气盐水在油酸导致的大鼠急性肺损伤(ALI)中的作用及其机制.方法 将健康成年SD大鼠80只随机分为4组:对照(Ⅰ)组、肺损伤(Ⅱ)组、肺损伤静脉H2干预(Ⅲ)组和肺损伤腹腔H2干预(Ⅳ)组,每组20只.检测血气分析;肺组织髓过氧化物酶(MPO)活性、丙二醛(MDA)以及肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)和NF-kB p65含量;并观察肺组织病理变化.结果 与注射油酸前比较,Ⅱ、Ⅲ和Ⅳ组在注射油酸3h后PaO2显著降低(P＜0.05).同时与Ⅰ组比较也存在PaO2显著降低(P＜0.05).此外,Ⅲ和Ⅳ组PaO2显著高于Ⅱ组(P＜0.05),且Ⅳ组PaO2高于Ⅲ组(P＜0.05).与Ⅰ组比较,Ⅱ组肺组织MPO活性及MDA水平显著增加(P＜0.01),Ⅲ和Ⅳ组肺组织MPO活性及MDA水平明显增加(P＜0.05),Ⅲ和Ⅳ组肺组织MPO活性及MDA水平与Ⅰ组比较显著降低(P＜0.05),且Ⅳ组肺组织MPO活性及MDA水平较Ⅲ组低(P＜0.05).Ⅱ、Ⅲ、Ⅳ组大鼠肺组织TNF-α、IL-1β和NF-κB p65水平明显高于Ⅰ组(P＜0.05).与Ⅱ组比较饱和氢气盐水治疗可降低油酸致肺损伤大鼠肺组织TNF-α、IL-1β和NF-κB p65水平(P＜0.05),且腹腔给药治疗较尾静脉给药治疗可更进一步降低油酸致肺损伤大鼠肺组织TNF-α、IL-1β和NF-κB p65水平(P＜0.05).结论 饱和氢气生理盐水能够降低大鼠油酸肺损伤模型中肺的损伤程度,且经腹腔注射给药效果更好,其机制可能与氢分子在体内的选择性抗氧化作用以及对肺组织内炎细胞浸润和炎症级联反应的抑制有关.     

外源性H2S吸入对大鼠肢体缺血／再灌注后心肌损伤的保护作用研究

目的 研究外源性H2S吸入对大鼠双下肢缺血/再灌注后心肌损伤的保护作用.方法 雄性Wistar大鼠23只,随机分为三组:①正常对照组( C组,8只);②缺血/再灌注组(I/R组,8只):应用止血带结扎构建大鼠双下肢缺血/再灌注模型,缺血4 h再灌注4 h.③H2S吸入组(H2S组,7只):大鼠双下肢缺血4 h,再灌注时给予含80 ppm H2S的合成空气持续吸入4 h.观察各组大鼠心肌病理、血浆H2S、肌酸激酶同工酶(CK-MB)、肌钙蛋白-T(TnT)、髓过氧化物酶(MPO)、肿瘤坏死因子-α(TNF-α)水平的变化及心肌胱硫醚-γ-裂解酶(CSE)活性、MPO、TNF-α水平的变化.以免疫组化法观察心肌细胞TNF-α的表达.结果 与C组比较,I/R组血浆CK-MB、TnT、MPO、TNF-α及心肌MPO、TNF-α水平明显上升(P＜0.05),血浆H2S及心肌CSE活性明显下降(P＜0.05),H2S吸入后血浆H2S及心肌CSE活性明显升高;同时,血浆CK-MB、TnT、MPO、TNF-α及心肌MPO、TNF-α水平明显降低(P＜0.05).心肌病理提示I/R组心肌明显肿胀、血管充血,心肌细胞间可见明显分叶核粒细胞浸润,红细胞漏出增多,H2S吸入后心肌损伤明显减轻.心肌TNF-α免疫组化提示I/R组心肌胞浆棕色染色颗粒较C组明显增多,H2S吸入后心肌胞浆棕色染色颗粒明显减少.结论 外源性H2S吸入可以通过降低炎细胞浸润及炎性细胞因子激活而对骨骼肌缺血/再灌注的心肌损伤发挥保护作用.     

硫化氢／胱硫醚-γ-裂解酶系统在肺缺血／再灌注损伤中的作用

目的 探讨硫化氢/胱硫醚-γ-裂解酶(H2S/CSE)系统在肺缺血/再灌注损伤(LIRI)中的作用.方法 将40只SD大鼠随机均分成假手术组、LIRI组、NaHS组、炔丙基甘氨酸(PPG)组4组.制备在体大鼠单肺原位LIRI模型.NaHS组和PPG组分别于制模前腹腔注射NaHS 28 μmol/kg或PPG 30 mg/kg;假手术组和LIRI组给予生理盐水0.5 ml.实验结束后取血,检测血浆H2S浓度、超氧化物歧化酶(SOD)、髓过氧化物酶(MPO)活性和丙二醛(MDA)含量;检测肺组织H2S含量、CSE活性和CSE mRNA表达水平;计算肺系数及肺泡损伤率(IAR);并观察肺组织病理改变.结果 与假手术组比较,LIRI组血浆和肺组织H2S水平、肺组织CSE活性和CSE mRNA表达均降低(均P<0.01),血浆SOD降低,MDA、MPO升高(均P<0.01);肺系数、IAR增高(均P<0.01);同时LIRI组肺组织有明显的病理改变.与LIRI组比较,预先给予NaHS组血浆和肺组织H2S水平、肺组织CSE活性和CSE mRNA表达均升高(均P<0.01),血浆SOD升高,MDA、MPO降低(均P<0.01),肺系数、IAR降低(均P<0.01);同时肺组织病理改变减轻.而预先给予PPG组则相反,可加重LIRI所致的肺损伤(P<0.05或P<0.01).结论 H2S/CSE系统功能下调参与LIRI的病理过程,预先给予NaHS对肺组织有保护作用.     

槲皮素对脓毒症急性肺损伤大鼠肿瘤坏死因子-α/白细胞介素-1β的影响

目的 观察槲皮素对脓毒症相关急性肺损伤(ALI)大鼠肿瘤坏死因子α(TNF-α)、白细胞介素-1β(IL-1β)的影响,以及槲皮素对脓毒症时的肺保护作用.方法 选用健康雄性Wistar大鼠35只,按随机数字表法分为对照组(5只)、模型组(10只)、槲皮素高剂量组(75mg/kg,10只)和槲皮素低剂量组(50mg/kg,10只).腹腔注射脂多糖(LPS)10mg/kg 2ml建立脓毒症ALI大鼠模型;对照组给予等量生理盐水.治疗组于制模前30min腹腔注射槲皮素.各组于制模后6、12、24h取血,采用酶联免疫吸附法(ELISA)检测血清中TNF-α,IL-1β含量;于制模后24h腹腔注射水合氯醛麻醉并处死大鼠,取肺组织行苏木素-伊红(HE)染色观察组织病理学改变,取肺叶测定肺组织湿/干重比值(W/D比值).结果 与对照组比较,模型组制模后6h血清TNF-α(ng/L),IL-1β(ng/L)含量即明显升高(TNF-α:73.00±0.28比28.48±0.26,IL-1β:46.30±0.21比28.38±1.07,均P<0.01),肺W/D比值明显升高(5.710±0.025比3.860±0.034,P<0.01);与模型组比较,槲皮素低、高剂量组制模后6h TNF-α,IL-1β含量即明显下降(TNF-α:55.52±0.31、57.76±0.27,IL-1β:39.47±9.65、41.83±0.16,均P<0.05),肺组织病理改变明显好转,肺W/D比值明显下降(4.810±0.036、4.900±0.029,均P<0.05),两治疗组间炎症介质比较差异无统计学意义;高剂量组肺组织病理损伤改善程度明显优于低剂量组.结论 槲皮素可下调大鼠血清TNF-α,IL-1β含量,对脓毒症ALI大鼠的肺组织起保护作用.     

痰热清注射液对急性肺损伤大鼠肺内炎症因子的影响

目的 研究痰热清注射液对内毒素性急性肺损伤(ALI)大鼠肺内炎症因子的影响。方法 清洁级健康SD雄性大鼠56只,随机（随机数字法）分为空白组、模型组、干预组。模型组、干预组分别给予内毒素(LPS)尾静脉注射,1h后,干预组给予痰热清注射液尾静脉注射。三组分别选取2,4,6h三个观察点,取支气管肺泡灌洗液(BALF)放射免疫法检测TNF-α,IL-1β,IL-8的含量及Wright-Giermsa染色计中性粒细胞的比例(ωPMN),并观察肺组织病理学变化及测湿干质量比值(W/D)。采用SPSS 17.0统计软件,以P＜0.05为差异具有统计学意义。结果2,4,6h三个观察点,模型组BALF中TNF-α,IL-1β,IL-8的含量及ωPMN较空白组明显升高(P＜0.05或P＜0.01),肺组织W/D明显增加(P＜0.01),且病理损伤程度明显重于空白组。干预组BALF中TNF-α,IL-1β,IL-8的含量及ωPMN较模型组明显降低(P＜0.05或P＜0.01),肺组织W/D明显减少(P＜0.01)且病理损伤程度明显轻于模型组。结论 痰热清注射液能抑制内毒素性急性肺损伤肺内炎症因子水平,减轻急性肺损伤程度。     

不同复苏液对创伤失血性休克大鼠血浆及肺组织TNF-α、IL-6及MPO的影响

目的探讨大鼠创伤失血性休克复苏时使用25%白蛋白与乳酸林格液对早期肺损伤的影响及可能机制。方法45只SD大鼠随机分为3组,假手术(Sham)组、林格液(RL)组和白蛋白(ALB)组复苏后2h取血并处死动物取肺组织测定TNF-α、IL-6表达及髓过氧化酶(MPO)活性和肺湿/干重(肺W/D)比值。结果各实验组休克复苏2h后血浆及肺泡灌洗液TNF-α、IL-6表达以及肺组织MPO活性、肺W/D比值均较Sham组高(P<0.05);ALB组复苏后维持MAP80~90mmHg所需液体较RL组明显减少(P<0.05);ALB组复苏后血浆及肺泡灌洗液TNF-α、IL-6表达以及肺组织MPO活性、肺W/D比值均较RL组低(P<0.05)。结论大鼠创伤失血性休克时血浆及肺组织TNF-α、IL-6表达及MPO活性增高,白蛋白复苏较乳酸林格液复苏肺组织损伤减轻。     

重组人促红细胞生成素对脓毒症大鼠肺脏的保护作用

目的 探讨重组人促红细胞生成素(recombinant human erythropoietin,rHuEPO)对内毒素所致大鼠脓毒症急性肺损伤的保护作用.方法 45只雄性SD大鼠随机(随机数字法)分为对照组、模型组、rHuEPO组,每组均15只.经静脉推注脂多糖LPS(6 mg/kg)复制急性肺损伤(ALI)的动物模型,rHuEPO组造模前60 min静脉推注rHuEPO (5000 U/kg),观察12 h后处死.留取颈动脉血及肺组织标本.测定氧和指数(OI)、动脉血氧分压(PaO2)、动脉血二氧化碳分压(PaCO2)、pH值.采用酶联免疫法(ELISA法)测定大鼠血清TNF-α、IL-6、iNOS的水平.在光镜和透射电镜下观察肺组织的病理形态学变化,并取右肺下叶计算肺湿/干质量比(W/D).结果 (1)血气分析:与对照组相比,脓毒症组及rHuEPO组大鼠动脉血PaO2、pH显著降低,PaCO2显著升高;与脓毒症组相比,rHuEPO组PaO2、pH显著升高及PaCO2显著降低,差异具有统计学意义(P＜0.05).(2)各组大鼠肺组织湿干质量比(W/D)变化:与对照组相比,脓毒症组及rHuEPO组肺组织W/D显著增加;与脓毒症组相比,rHuEPO组肺组织W/D显著降低,差异具有统计学意义(P＜0.05).(3)各组大鼠12 h血清TNF-α、IL-6、iNOS水平的变化:脓毒症组及rHuEPO组上述指标明显高于对照组;与脓毒症组相比,rHuEPO组上述指标明显降低,差异具有统计学意义(P＜0.01).(4)光镜及电镜观察脓毒症组病理学改变为急性弥漫性肺损伤,表现为肺泡腔内出血、渗出、炎性细胞浸润,肺微血管内皮细胞、Ⅰ型和Ⅱ型上皮细胞坏死;rHuEPO组急性肺损伤明显轻于脓毒症组,只可见到局灶性肺泡少量炎性细胞浸润.结论 rHuEPO能够降低血清TNF-α、IL-6、iNOS水平进而调节炎症反应,对脓毒症所致急性肺损伤具有一定的保护作用.     

亚低温对ARDS大鼠肺部炎症反应影响的研究

目的 探讨亚低温对大鼠内毒素性急性呼吸窘迫综合征(ARDS)肺部炎症反应的影响.方法 大鼠腹腔注射内毒素(LPS,1 mg/kg),16 h后再气管内滴注LPS(3 mg/kg)建立ARDS模型.72只雄性SD大鼠随机分为3组:对照组(C组)、ARDS组(A组)、亚低温组(M组),分别于ARDS时及ARDS后2、4、6 h处死动物,观察肺组织病理形态;计算肺湿质量/干质量(W/D)比值;检测肺组织中TNF-α、IL-8、IL-1β、IL-6含量.结果 3组动物肺组织病理形态有明显的不同.肺W/D:A组、M组均明显高于C组(P<0.01),M组较A组明显降低(P<0.01).肺组织TNF-α、IL-8、IL-1β、IL-6含量:A组、M组明显高于C组(P<0.01),M组明显低于A组(P<0.01).结论 亚低温治疗可减轻内毒素性ARDS大鼠肺部炎症反应.     

地塞米松联合依达拉奉对百草枯中毒所致大鼠急性肺损伤模型的救治

目的:观察地塞米松联合依达拉奉对百草枯中毒诱导的大鼠急性肺损伤(ALI)模型的治疗效果。方法:取健康成年雄性SD大鼠120只,随机分为生理盐水组(NS组)、百草枯组(PQ组)、百草枯+地塞米松组(实验1组),百草枯+地塞米松+依达拉奉组(实验2组),每组各30只。百草枯ALI模型,由百草枯溶液20mg/kg单次尾静脉注射制备;NS组则以等体积的生理盐水尾静脉注射所制。实验组是在百草枯模型成功制备1h后,以相应的药物处理得到,实验1组:在百草枯模型上予地塞米松1mg/kg腹腔注射所制;实验2组:在百草枯模型上给予地塞米松1mg/kg+依达拉奉3mg/kg腹腔注射所致。给药5h后处死大鼠,比较各组大鼠肺泡灌洗液中炎性细胞的数目、肺组织湿/干(W/D)、RT-PCR法检测肺组织中TNF-αmRNA及ELISA法检测血清中IL-1β、IL-8的水平。结果:PQ组肺泡灌洗液中炎性细胞数目、肺组织W/D、肺组织中TNF-αmRNA及血清中IL-1β、IL-8的水平均高于NS组(P0.01);实验1、2组中的各项指标均低于PQ组(P0.05、P0.01);相较于实验1组,实验2组中肺泡灌洗液中炎性细胞数目、肺组织W/D均明显下降(P0.01),肺组织中TNF-αmRNA及血清中IL-1β、IL-8的水平下降(P0.05)。结论:地塞米松可缓解百草枯中毒所致的ALI,而联合依达拉奉,可增强这种保护作用。     

The clearance of Procalcitonin (PCT) during continuous veno-venous hemodiafiltration (CVVHD)

Objective. To evaluate the Procalcitonin (PCT) clearance during continuous veno-venous hemodiafiltration (CVVHD).?Design. Case report?Setting. Surgical intensive care unit?Patient. 51-year-old man, who had undergone total thyroidectomy about ten years before owing to multiple endocrine neoplasia 2 (MEN 2), suffering from multiple organ dysfunction syndrome (MODS) with acute renal failure after severe trauma caused by a traffic accident.?Measurements and main result. The samplings of prefilter (afferent) and post-filter (efferent) blood and of ultradiafiltrate were 6 times performed during 24 h of CVVHD to calculate the PCT clearance of hemdiafiltration.?During the first half period of CVVHD the serum PCT concentration did not decrease, though PCT had been eliminated from serum. On the other hand during the latter half period of it the serum PCT value decreased (from 46.8 ng/ml to 29.4 ng/ml) and the amount of the eliminated PCT from serum was about 100 ng per minute and its clearance was 2.3 ∼ 3.4 ml/min.?Conclusion. The CVVHD could eliminate PCT from serum. First it was brought about by the adsorption by the filter menbrane and then by ultradiafiltration. Received: 25 February 1999/Final revision received: 31 May 1999/Accepted: 9 June 1999     

Ultrasonic study of venous patterns in the right hypochondrium: An anatomical approach to differential diagnosis of obstructive jaundice

Through real time ultrasonography, it is possible to display the splenic vein, the superior mesenteric vein, the vena porta, and the intrahepatic portal and systemic veins. In jaundice, it is of the utmost importance to carefully identify the vena porta before making a diagnosis of common bile duct enlargement. It is also necessary, when confronted with a pattern of apparently enlarged intrahepatic ducts, to conduct a thorough study of possible confluences of the ducts with the vena porta or vena cava to be certain that the ducts are not part of the portal or systemic venous network. Without such differentiation, portal enlargement caused portal hypertension, systemic venous enlargement caused cardiac insufficiency, or even nonpathological wide veins may lead to an erroneous diagnosis of obstructive jaundice.     

人工通气在非心脏疾患致心搏呼吸骤停心肺脑复苏中价值的探讨

目的　评价人工气道建立和有效通气在非心脏疾患引起心搏骤停患者心肺脑复苏 (CPCR)中的真正价值 ,分析与总结有效人工通气与Ⅰ、Ⅱ、Ⅲ期复苏成功率之间关系 ,探讨对这类患者采取CPCR的抢救步骤和时机 ,为临床采取切实有效CPCR步骤提供依据。方法　选择非单纯心脏疾患致心搏呼吸停止行CPCR患者 2 6例作为分析对象。按照心肺复苏(CPR)实际操作过程中所采取的方法不同 ,将患者分为CAB组 (12例 / 12例次 )和ABC组 (14例 / 18例次 )。CAB组中 ,按照C与AB步骤采取的间隔时间不同 ,分为 <5min、5～ 10min、>10min组 ;ABC组中 ,部分患者在发生心搏骤停以前 ,已经建立人工气道和接受有效通气治疗 ,一旦心搏骤停发生后 ,在AB措施已经存在条件下进行心脏复苏。统计与计算各组复苏成功率(% ) ,χ2 检验各组差异显著性。结果　CAB组患者接受C -AB间隔时间不等 ,Ⅰ、Ⅱ期复苏成功率无显著差异 ,但Ⅲ期复苏成功率差异显著 (P <0 0 5 )。ABC组Ⅲ期复苏成功率分别为 83 3% (15 / 18)、77 7% (14 / 18)、6 6 7% (12 / 18) ,与CAB组总体比较无显著差异 (P >0 0 5 )。结论　虽然CAB对非单纯心脏疾患致心搏呼吸骤停的患者也是可取的CPCR抢救步骤 ,但及时建立人工气道进行有效通气仍是不可忽视的重要步骤 ,尤其当 5min内     

动脉瘤性蛛网膜下腔出血病人血清FSH LH PRL GH的浓度变化

目的　研究动脉瘤性蛛网膜下腔出血 (SAH)病人血清卵泡刺激素 (FSH)、黄体生成素 (LH)、泌乳素 (PRL)、生长激素 (GH)的浓度变化规律。方法　对 35例动脉瘤性SAH病人发病后 1～ 3、7～ 9、13～ 15d血清FSH、LH、PRL、GH的浓度进行动态观察 ,用TCD检测大脑中动脉血流速度 (VMCA)。结果　动脉瘤性SAH病人血清FSH、LH、PRL、GH浓度在发病后 1～3、7～ 9d各均值明显高于对照组 ,尤以发病后 7～ 9d变化最明显 ;术前、术后有脑血管痉挛 (CVS)组和非CVS组也有明显差异。结论　动脉瘤性SAH病人血清FSH、LH、GH、PRL含量与SAH的病情演变、CVS程度有关 ,并可判断预后。     

Creatine kinase and myoglobin determination in myocardial infarction

Summary In order to evaluate the diagnostic and prognostic impertance of serum myoglobin (Mb) determination during acute myocardial infarction (AMI) we determined the time of first rise of both CK and Mb, that is the time in hours between the onset of pain and the last normal myoglobin and enzyme determination (TFR for Mb=2.2±1.5 h; TFR for CK=4.0±2.5 h). We also attempted to evaluate infarct size by mathematical analysis of the serum concentrations of Mb. The average percentage difference between the infarct size calculated from the CK concentrations and Mb concentrations was 35.8±35.2%. The results show that the determination of serum myoglobin is a useful and sensitive test for the early diagnosis of AMI. On the other hand, the serum myoglobin cannot be utilized to evaluate infarct size. The main limitation in the determination of infarct size from the serum Mb concentrations lies in the extreme variability of the disappearance rate (Kd), mainly resulting from the renal elimination of the substance.     

Quality management of potential chemotherapy-induced neutropenic complications: evaluation of practice in an academic medical center

Goals

Management of the risk of potential chemotherapy-induced neutropenic complications such as febrile neutropenia (FN) and severe neutropenia (SN) is a quality of care priority. How frequently does care at our institution conform to established guidelines?

Materials and methods

This retrospective chart review study included a random sample of 305 cancer patients receiving care at a single US academic medical center. Abstracted data included demographics, risk factors, and outcome variables (e.g., development of FN/SN, administration of myeloid growth factors). To evaluate quality of care, we assessed conformance between actual practice and established clinical practice guidelines for the use of myeloid growth factors from the National Comprehensive Cancer Network (NCCN).

Main results

Of the 305 cases reviewed, 8% were classified as low risk (<10%), 48% as intermediate risk (10–20%), and 44% as high risk (>20%), using the risk classifications in the NCCN guidelines modified to accommodate illness and other risk factors. Thirty-four percent received prophylactic administration of myeloid growth factors. Half of the cases had adequate documentation of mid-cycle absolute neutrophil count to determine whether FN/SN developed. Among these cases with adequate documentation, 21% developed FN/SN. Use of growth factors did not conform to established quality guidelines. Overall, 77 of 133 (58%) high-risk cases received myeloid growth factors, whereas six of 25 (24%) low-risk cases received myeloid growth factors.

Conclusions

Routine clinical practice in this academic oncology setting was poorly aligned with established guidelines; there is substantial opportunity to standardize clinical strategies and increase conformance with evidence-based guidelines.     

颅脑外伤急性期血清镁离子浓度的变化

目的 探讨急性颅脑外伤（ACI）患者血清镁离子浓度变化特点及其对脑细胞功能代谢的影响.方法 85例ACI患者,GCS＞8分35例,GCS≤8分50例,测定血清镁离子浓度、钙离子浓度、脑血管痉挛发生率、脑血氧饱和度.观察低镁血症患者一个月后GOS预后评分及外源性硫酸镁的临床疗效.结果 85例ACI患者血清镁离子浓度明显低于30例正常对照组患者,且降低程度与脑伤程度呈正相关;GCS≤8分者低镁血症发生率明显高于GCS＞8分者;低镁血症患者其脑血管痉挛发生率明显高于对照组,脑血氧饱和度明显低于对照组,GOS评分≤3分者明显多于对照组;24 h内给予硫酸镁能明显提高GOS评分.结论 镁离子浓度的降低直接参与了ACI时继发性脑损害,与伤情及预后密切相关.早期给予硫酸镁对脑组织有明确的保护作用,且它价廉、安全,来源丰富,故有广泛应用前景.     

Low-Intensity Ultrasound Reduces High Glucose-Induced Nitric Oxide Generation in Retinal Pigment Epithelial Cells

Diabetic retinopathy (DR) is a severe micro-vascular complication of diabetes. High glucose (HG)-evoked nitric oxide (NO) production mediated by increased oxidative stress is a key factor in DR pathogenesis. In this study, we examined whether low-intensity ultrasound (LIUS) stimulation can reduce HG-induced NO generation. We determined that LIUS stimulation decreased the HG-induced NO generation possibly via inhibition of reactive oxygen species (ROS) and subsequently diminished the associated pro-inflammatory pathway involving the induced expression of inducible nitric oxide synthase, cyclooxygenase-2 and vascular endothelial growth factor. In addition, we determined that LIUS stimulation reduced the quantity of NO produced by N-acetylcysteine, which was not mediated by ROS. These results indicate that LIUS can inhibit both ROS-dependent and -independent NO generation processes in ARPE-19 cells. We envision LIUS as a potential therapeutic alternative to treat DR. Further studies are required to understand the underlying mechanism of the LIUS-induced reduction of NO generation for DR therapy.