吗啡预处理-后处理对大鼠离体心脏缺血再灌注损伤的影响

Objective To evaluate the effects of morphine preconditioning-postconditioning on ischemia-reperfusion (I/R) injury in isolated rat hearts. Methods Male SD rats weighing 180-200 g were killed after intraperitoneal injection of heparin 500 U/kg. The hearts were immediately removed and perfused in a Langendorff apparatus with K-H solution gassed with 95%O2-5%CO2 .HR and left ventricular systolic pressure (LVSP) were measured from a fluid-filled latex balloon in the left ventricle. Global myocardial ischemia was induced by interrupting perfusion for 45 min followed by 60 min reperfusion. Forty isolated rat hearts were randomly divided into 5 groups (n = 8 each): group 1 (I/R); group II morphine preconditioning (M1 ); group Ⅲ morphine postconditioning (M2); group IV M1 + M2; group V 5-hydroxydecanoate (5-HD) + M2. Group M1 was perfused with K-H solution containing morphine 3.0 μmol/L for 20 min 30 min before ischemia followed by 10 min normal K-H solution perfusion. Group M2 was perfused with K-H solution containing morphine 3.0 μmol/L for 10 min at the beginning of reperfusion followed by 50 min normal K-H solution perfusion. Group 5-HD + M2 was perfused with K-H solution containing morphine 3.0 μmol/L+ 5-HD 10-4 mmol/L for 10 min at the beginning of reperfusion followed by 50 min normal K-H solution perfusion. Myocardial CK-MB activity was measured and myocardial infarct size (IS/AAR) detennined (by 2,3,5-triphenyl tetrazolium staining) at the end of 60 min reperfusion. Results The preconditioning, postconditioning and combination of preconditioning and postconditioning with morphine 3.0 μmol/L perfusion for 10 min all provided cardio-protective effects in terms of IS/AAR and myocardial activation of CK-MB. Conclusion Although the combination of morphine preconditioning and postconditioning can protect the heart against I/R injury, the effects are similar to those of either of them alone, and the reason may be that either of them alone protects the heart against I/R injury via activating mitoKATP .     

吗啡预处理-后处理对大鼠离体心脏缺血再灌注损伤的影响

Objective To evaluate the effects of morphine preconditioning-postconditioning on ischemia-reperfusion (I/R) injury in isolated rat hearts. Methods Male SD rats weighing 180-200 g were killed after intraperitoneal injection of heparin 500 U/kg. The hearts were immediately removed and perfused in a Langendorff apparatus with K-H solution gassed with 95%O2-5%CO2 .HR and left ventricular systolic pressure (LVSP) were measured from a fluid-filled latex balloon in the left ventricle. Global myocardial ischemia was induced by interrupting perfusion for 45 min followed by 60 min reperfusion. Forty isolated rat hearts were randomly divided into 5 groups (n = 8 each): group 1 (I/R); group II morphine preconditioning (M1 ); group Ⅲ morphine postconditioning (M2); group IV M1 + M2; group V 5-hydroxydecanoate (5-HD) + M2. Group M1 was perfused with K-H solution containing morphine 3.0 μmol/L for 20 min 30 min before ischemia followed by 10 min normal K-H solution perfusion. Group M2 was perfused with K-H solution containing morphine 3.0 μmol/L for 10 min at the beginning of reperfusion followed by 50 min normal K-H solution perfusion. Group 5-HD + M2 was perfused with K-H solution containing morphine 3.0 μmol/L+ 5-HD 10-4 mmol/L for 10 min at the beginning of reperfusion followed by 50 min normal K-H solution perfusion. Myocardial CK-MB activity was measured and myocardial infarct size (IS/AAR) detennined (by 2,3,5-triphenyl tetrazolium staining) at the end of 60 min reperfusion. Results The preconditioning, postconditioning and combination of preconditioning and postconditioning with morphine 3.0 μmol/L perfusion for 10 min all provided cardio-protective effects in terms of IS/AAR and myocardial activation of CK-MB. Conclusion Although the combination of morphine preconditioning and postconditioning can protect the heart against I/R injury, the effects are similar to those of either of them alone, and the reason may be that either of them alone protects the heart against I/R injury via activating mitoKATP .     

沂蒙山区3年32例阿尔茨海默病患者淀粉样β蛋白及其前体基因表达量的相关性分析

背景:淀粉样β蛋白沉积是引致阿尔茨海默病的重要原因,淀粉样β蛋白前体基因过度表达或某部分发生突变,可能与阿尔茨海默病的发生有关。目的:观察沂蒙山区阿尔茨海默病与淀粉样β蛋白及其前体基因的关系。设计:病例-对照分析。单位:临沂市人民医院神经内科。对象:选择临沂医专附属临沂市人民医院神经内科2001-01/2003-12住院阿尔茨海默病患者32例,以性别、年龄相当的非颅脑损伤的外科手术老年人30例为对照组(简易精神状态量表评分>27分)。方法:应用ELISA法检测脑脊液淀粉样β蛋白水平,应用荧光定量聚合酶链反应技术检测淀粉样β蛋白前体基因表达量。结果:62例全部进入结果分析。①阿尔茨海默病组脑脊液淀粉样β蛋白水平明显高于对照组[(13.63±9.34),(6.75±5.37)μg/L,t=3.354,P<0.01]。②阿尔茨海默病组脑脊液淀粉样β蛋白前体表达量明显高于对照组[(1624±298),(1275±269)拷贝/μL,t=4.42,P<0.01]。③阿尔茨海默病组淀粉样β蛋白水平与淀粉样β蛋白前体基因表达量呈正相关(r=0.44,P<0.01)。结论:沂蒙山区阿尔茨海默病患者脑脊液中淀粉样β蛋白及其前体基因表达增高,且淀粉样β蛋白水平越高,其前体基因表达越高,痴呆程度越重。提示阿尔茨海默病与淀粉样β蛋白、淀粉样β蛋白前体密切相关。但淀粉样β蛋白前体表达量在阿尔茨海默病诊断中不具特异性。     

吸入麻醉与术后躁动

全麻术后苏醒期患者躁动的危害性极大,其诱发因素很多,其中吸入麻醉可能是主要原因。中枢局灶敏感化是吸入麻醉诱发躁动的可能机制,这种功能完整性的缺失影响患者对感觉的反应和处理能力,在某些有害刺激的作用下,中枢神经系统表现为过度兴奋而诱发躁动。预防和治疗术后躁动的方法包括药物性和非药物性处理措施。     

沂蒙山区3年32例阿尔茨海默病患者淀粉样β蛋白及其前体基因表达量的相关性分析

背景：淀粉样β蛋白沉积是引致阿尔茨海默病的重要原因，淀粉样β蛋白前体基因过度表达或某部分发生突变，可能与阿尔茨海默病的发生有关。目的：观察沂蒙山区阿尔茨海默病与淀粉样β蛋白及其前体基因的关系。设计：病例-对照分析。单位：临沂市人民医院神经内科。对象：选择临沂医专附属临沂市人民医院神经内科2001-01／2003-12住院阿尔茨海默病患者32例，以性别、年龄相当的非颅脑损伤的外科手术老年人30例为对照组（简易精神状态量表评分〉27分）。方法：应用ELISA法检测脑脊液淀粉样β蛋白水平，应用荧光定量聚合酶链反应技术检测淀粉样β蛋白前体基因表达量。结果：62例全部进入结果分析。①阿尔茨海默病组脑脊液淀粉样β蛋白水平明显高于对照组[（13．63&;#177;9．34），（6．75&;#177;5．37）μg／L，t=3．354,P〈0．01]。②阿尔茨海默病组脑脊液淀粉样B蛋白前体表达量明显高于对照组[（1624&;#177;298），（1275&;#177;269）拷贝／μL。t=4．42，P〈0．01]。③阿尔茨海默病组淀粉样β蛋白水平与淀粉样β蛋白前体基因表达量呈正相关（r=0．44，P〈0．01）。结论：沂蒙山区阿尔茨海默病患者脑脊液中淀粉样β蛋白及其前体基因表达增高，且淀粉样β蛋白水平越高，其前体基因表达越高。痴呆程度越重。提示阿尔茨海默病与淀粉样β蛋白、淀粉样β蛋白前体密切相关。但淀粉样β蛋白前体表达量在阿尔茨海默病诊断中不具特异性。     

吗啡后处理对大鼠离体心脏缺血再灌注损伤的影响

目的 评价吗啡后处理对大鼠离体心脏缺血再灌注损伤的影响.方法 雄性SD大鼠,体重180～200 g,应用Langendorff灌流装置,采用全心停灌45 min、再灌注60 min的方法制备大鼠离体心脏缺血再灌注模型.实验一:取模型制备成功的心脏32个,随机分为4组(n=8):Ⅰ组～Ⅳ组,Ⅰ组不予处理,Ⅱ组～Ⅳ组于再灌注即刻分别灌注含0.3、3.0和30 μmol/L吗啡的K-H液10 min,随后灌注正常K-H液50 min;实验二:根据实验一的结果,选择对离体心脏缺血再灌注损伤影响最强的吗啡浓度,另取模型制备成功的心脏32个,随机分为4组(n=8):Ⅰ组～Ⅳ组,Ⅰ组不予处理,Ⅱ组～Ⅳ组于再灌注即刻分别灌注含吗啡的K-H液5、10和20 min,随后灌注正常K-H液50 min;实验三:根据实验二的结果,选取对离体心脏缺血再灌注损伤影响最强的吗啡后处理方法.另取模型制备成功的心脏37个,随机分为5组:Ⅰ组(n=8)不予处理;Ⅱ组(n=8)、Ⅲ组～Ⅴ组(n=7)于再灌注即刻分别灌注含吗啡、10 μmol/L非选择性阿片受体阻断剂纳洛酮和吗啡、5 μmol/L选择性κ受体阻断剂nor-binahorphimine和吗啡、5 μmol/L选择性δ受体阻断剂naltrindole和吗啡的K-H液,各组均再灌注正常K-H液50 min.于再灌注60 min时测定心肌肌酸激酶同工酶(CK-MB)活性,计算心肌缺血危险区/梗塞区(IS/AAR).结果 根据实验一、二的结果于再灌注即刻灌注含3.0 μmol/L吗啡的K-H液10 min行后处理.实验三的结果:与Ⅰ组比较,Ⅱ组和Ⅴ组心肌IS/AAR和CK-MB活性降低,Ⅳ组心肌CK-MB活性降低(P<0.05或0.01),Ⅲ组以上指标差异无统计学意义(P>0.05);与Ⅱ组比较,Ⅲ组和Ⅳ组心肌IS/AAR和CK-MB活性升高(P<0.01),Ⅴ组上述指标差异无统计学意义(P>0.05).结论 吗啡后处理可减轻大鼠离体心脏缺血再灌注损伤,此作用可能与激活心肌κ受体有关.     

异丙酚对瓣膜置换病人颅内血浆氨基酸代谢的影响

本研究观测体外循环(CPB)期间谷氨酸(Glu)、γ-氨基丁酸(GABA)的变化,及异丙酚对Glu、GABA释放的影响。资料与方法选32例心脏瓣膜置换术病人,男17例,女15例,年龄24～72岁,体重45～72kg,心功能Ⅱ～Ⅲ级。随机分为观察组16例,CPB开始时用微量泵按4mg·kg-1·h-1泵入异丙酚,至CPB结束。对照组16例,CPB中不用异丙酚。     

术中持续静脉注射利多卡因对胸腔镜肺叶切除术患者术中麻醉用药及术后疼痛的影响

目的:探讨利多卡因对胸腔镜肺叶切除术患者术中药物用量、术后恢复质量和术后慢性疼痛（postoperative chronic pain, CPSP）的影响。方法:纳入择期胸腔镜下肺叶切除术患者90例,采用随机数字表法将患者分为利多卡因组（L组）和对照组（C组）,每组45例。L组麻醉诱导时给予利多卡因1.0 mg/kg,...     

三种围手术期镇痛方法对子宫颈癌患者细胞免疫功能的影响

手术可引起细胞因子的释放,这些促炎细胞因子进而可促使其他炎性介质的释放,并刺激外周前列腺素(PG)的合成,创伤部位局部也释放PGE2,这些炎性介质的释放可抑制细胞免疫功能[1-2].临床中常用阿片类物质缓解手术疼痛,其本身也可导致细胞免疫抑制[3].研究表明,PGE2参与了肿瘤细胞转化和生殖道肿瘤的形成[1].     

吗啡预处理-后处理对大鼠离体心脏缺血再灌注损伤的影响

Objective To evaluate the effects of morphine preconditioning-postconditioning on ischemia-reperfusion (I/R) injury in isolated rat hearts. Methods Male SD rats weighing 180-200 g were killed after intraperitoneal injection of heparin 500 U/kg. The hearts were immediately removed and perfused in a Langendorff apparatus with K-H solution gassed with 95%O2-5%CO2 .HR and left ventricular systolic pressure (LVSP) were measured from a fluid-filled latex balloon in the left ventricle. Global myocardial ischemia was induced by interrupting perfusion for 45 min followed by 60 min reperfusion. Forty isolated rat hearts were randomly divided into 5 groups (n = 8 each): group 1 (I/R); group II morphine preconditioning (M1 ); group Ⅲ morphine postconditioning (M2); group IV M1 + M2; group V 5-hydroxydecanoate (5-HD) + M2. Group M1 was perfused with K-H solution containing morphine 3.0 μmol/L for 20 min 30 min before ischemia followed by 10 min normal K-H solution perfusion. Group M2 was perfused with K-H solution containing morphine 3.0 μmol/L for 10 min at the beginning of reperfusion followed by 50 min normal K-H solution perfusion. Group 5-HD + M2 was perfused with K-H solution containing morphine 3.0 μmol/L+ 5-HD 10-4 mmol/L for 10 min at the beginning of reperfusion followed by 50 min normal K-H solution perfusion. Myocardial CK-MB activity was measured and myocardial infarct size (IS/AAR) detennined (by 2,3,5-triphenyl tetrazolium staining) at the end of 60 min reperfusion. Results The preconditioning, postconditioning and combination of preconditioning and postconditioning with morphine 3.0 μmol/L perfusion for 10 min all provided cardio-protective effects in terms of IS/AAR and myocardial activation of CK-MB. Conclusion Although the combination of morphine preconditioning and postconditioning can protect the heart against I/R injury, the effects are similar to those of either of them alone, and the reason may be that either of them alone protects the heart against I/R injury via activating mitoKATP .