异丙酚诱导,普鲁卡因静脉复合液维持麻醉对颅内压,脑灌注…

１１例颅内压增高行颅内肿瘤切除术患者，用异丙酚２ｍｇ／ｋｇ诱导，普鲁卡因静脉复合液维持麻醉，按普鲁卡因１ｍｇ／ｋｇ／ｍｉｎ滴入，诱导前，后共３５ｍｉｎ，观察ＭＡＰ，ＩＣＰ，ＣＰＰ变化，结果发现：异丙酚可使ＩＣＰ迅速显著降低（Ｐ〈０．０１）；诱导开始插管后，ＣＰＰ无显著变化（Ｐ〈０．０５），插管１０ｍｉｎ后有显著升高，结果认为：异丙酚可使高颅压患者ＩＣＰ迅速显著下降，普鲁卡因维持麻醉，可较好地维持循     

Erythropoietin inhibits angiotensin Ⅱ induced cardiomyocyte hypertrophy in vitro via activating PI3K/Akt-eNOS pathway

Objective To explore the effect of erythropoietin (EPO) on angiotensin Ⅱ (Ang Ⅱ) induced neonatal rat cardiomyocyte hypertrophy and the association with PI3K/Akt-eNOS signaling pathway. Methods Cardiomyocytes were isolated from new-born Sprague-Dawley rats and stimulated by Ang Ⅱ in vitro. The cell surface area and mRNA expression of atrial natriuretic factor (ANF) of cardiomyocytes were determined in the presence and absence of various concentrations of EPO, phosphatidylinositol 3'-kinase (PI3K) inhibitor LY294002 and nitric oxide synthase (NOS) inhibitor L-NAME. Intracellular signal molecules, such as Akt, phosphorylated Akt, eNOS and phosphorylated eNOS protein expressions were detected by western blot. Nitric oxide (NO) level in the supernatant of cultured cardiomyocytes was assayed by NO assay kit. Results EPO (20 U/ml) significantly inhibited Ang Ⅱ induced cardiomyocyte hypertrophy as shown by decreased cell surface area and ANF mRNA expression (all P ＜0.05). EPO also activated Akt and enhanced the expression of eNOS and its phosphorylation (all P ＜ 0.05), increased the NO production (P ＜0.01). These effects could be partially abolished by cotreatment with LY294002 or L-NAME (all P ＜ 0.05). Conclusion EPO attenuates Ang Ⅱ induced cardiomyocytes hypertrophy via activating PI3K-Akt-eNOS pathway and promoting NO production.     

促红细胞生成素对培养的乳鼠心肌细胞肥大的影响

目的:观察促红细胞生成素(EPO)对乳鼠心肌细胞肥大的影响.方法:体外分离培养乳鼠心肌细胞,用血管紧张素Ⅱ(AngⅡ)刺激产生肥大的心肌细胞,加入不同浓度的EPO对肥大心肌细胞进行干预,以细胞表面积和心钠素(ANF)mRNA表达作为细胞肥大的观察指标,采用Western blot方法检测细胞内信号分子转化生长因子β1(TGF-β1)、Smad2及p-Smad2蛋白表达.结果:20U/ml的EPO能有效逆转AngⅡ诱导的心肌细胞肥大,低于此浓度未见明显效果;EPO能减弱促心肌细胞肥大信号分子TGF-β1、Smad2 及p-Smad2蛋白表达.结论:EPO具有抗心肌细胞肥大作用,且这一作用与TGF-β1-Smad2信号途径有关.     

促红细胞生成素对乳鼠心肌细胞肥大及P13K/Akt-eNOS信号转导通路的影响

目的 探讨促红细胞生成素(EPO)对血管紧张素Ⅱ(AngⅡ)诱导的肥大心肌细胞的影响,以及磷脂酰肌醇3激酶(PI3K)/丝氨酸苏氨酸激酶(Akt)-内皮型一氧化氮合酶(eNOS)信号转导通路在其中的作用.方法 分离乳鼠心肌细胞,利用AngⅡ诱导建立心肌细胞肥大模型,以心肌细胞表面积和心钠素(ANF)mRNA表达作为心肌细胞肥大观察指标.观察不同浓度EPO对肥大心肌细胞的影响,并利用PI3K抑制剂LY294002和一氧化氮合酶抑制剂L-NAME对其相关机制进行探讨,I司时对细胞培养液中一氧化氮(NO)浓度进行检测,蛋白免疫印迹法检测磷酸化Akt(p-Akt)、Akt、磷酸化eNOS(p-eNOS)和eNOS蛋白表达情况.结果 20 U/ml EPO能抑制由AngⅡ诱导的心肌细胞肥大,表现为心肌细胞表面积和ANF mRNA表达均减少(P＜0.05).EPO能激活Akt,促进eNOS及p-eNOS表达增加(均P＜0.05),并使NO合成增加(P＜0.01).LY294002和L-NAME能逆转EPO的抗心肌细胞肥大作用,减少NO产最(P＜0.05).蛋白免疫印迹法榆测显示,LY294002能够抑制EPO对p-Akt、p-eNOS和eNOS蛋白表达的促进作用,而L-NAME能抑制eNOS的磷酸化(均P＜0.05).结论 EPO能够抑制AngⅡ诱导的心肌细胞肥大,该作用可能是通过激活P13K/Akt信号转导通路,促进eNOS表达与活化,从而促进NO的合成来实现的.     

小儿寰枢关节半脱位的诊断及治疗

临床上小儿寰枢关节半脱位较少见,一般表现为突发颈痛、斜颈、活动受限,容易与肌性、骨性、视力障碍性斜颈相混淆,往往容易漏诊、误诊而延误治疗。早期正确诊疗预后较好,延误诊治可残留颈部强直和颅底宽畸形。2008年7月至2011年4月,我科共收治了11例小儿寰枢关节半脱位患者,体会如下。1资料与方法     

Erythropoietin inhibits angiotensin Ⅱ induced cardiomyocyte hypertrophy in vitro via activating PI3K/Akt-eNOS pathway

Objective To explore the effect of erythropoietin (EPO) on angiotensin Ⅱ (Ang Ⅱ) induced neonatal rat cardiomyocyte hypertrophy and the association with PI3K/Akt-eNOS signaling pathway. Methods Cardiomyocytes were isolated from new-born Sprague-Dawley rats and stimulated by Ang Ⅱ in vitro. The cell surface area and mRNA expression of atrial natriuretic factor (ANF) of cardiomyocytes were determined in the presence and absence of various concentrations of EPO, phosphatidylinositol 3'-kinase (PI3K) inhibitor LY294002 and nitric oxide synthase (NOS) inhibitor L-NAME. Intracellular signal molecules, such as Akt, phosphorylated Akt, eNOS and phosphorylated eNOS protein expressions were detected by western blot. Nitric oxide (NO) level in the supernatant of cultured cardiomyocytes was assayed by NO assay kit. Results EPO (20 U/ml) significantly inhibited Ang Ⅱ induced cardiomyocyte hypertrophy as shown by decreased cell surface area and ANF mRNA expression (all P ＜0.05). EPO also activated Akt and enhanced the expression of eNOS and its phosphorylation (all P ＜ 0.05), increased the NO production (P ＜0.01). These effects could be partially abolished by cotreatment with LY294002 or L-NAME (all P ＜ 0.05). Conclusion EPO attenuates Ang Ⅱ induced cardiomyocytes hypertrophy via activating PI3K-Akt-eNOS pathway and promoting NO production.     

NF-κB介导ADMA上调大鼠腹腔巨噬细胞LOX-1的表达

目的 探讨非对称性二甲基精氨酸(ADMA)上调大鼠腹腔巨噬细胞的氧化低密度脂蛋白受体-1(LOX-1)表达是否受核因子-κB(NF-κB)的调控.方法 分离培养大鼠腹腔巨噬细胞.实验分组:正常对照组,以含10%胎牛血清(FBS)DMEM培养液与巨噬细胞共孵育;氧化型低密度脂蛋白(oxLDL)组,在培养液中加oxLDL(50 mg/L);A+O组,在培养液中加ADMA(15 μmol/L)和oxLDL(50 mg/L);P+A+O组,在培养液中加吡咯烷二硫代氨基甲酸盐(PDTC,25 μmol/L)、ADMA(15 μmol/L)、oxLDL(50 mg/L).以实时荧光定量PCR(Real-time PCR)和Western blot分别检测LOX-1 mRNA和蛋白表达,以电泳迁移率变动分析(EMSA)和增强化学发光法(ECL)检测NF-κB活性.结果 oxLDL组与A+O组LOX-1 mRNA和蛋白表达比对照组明显增强,以A+O组尤为明显(均 P ＜0.05);P+A+O组LOX-1 mRNA和蛋白表达较A+O组降低(P ＜0.05).与对照组相比,oxLDL组与A+O组NF-κB活性明显增强,以A+O组尤为明显(均 P ＜0.05);P+A+O组NF-κB活性较A+O组降低(P ＜0.05).相关分析:NF-κB活性与LOX-1 mRNA和蛋白表达量呈正相关(均为 r =0.82,P ＜0.05).结论 ADMA可能通过NF-κB途径增强LOX-1表达而促进巨噬细胞转化为泡沫细胞,促进动脉粥样硬化的发生发展.     

体外诱导间充质干细胞向心肌细胞分化的研究进展

间充质干细胞是近年来一类倍受人们关注的干细胞,它有望成为心脏组织修复工程最理想的种子细胞。多项研究表明,间充质干细胞能在体外被诱导分化为心肌细胞,但是与其分化的相关因素和分化机制还需要进一步的研究探讨。     

Clinical Significance of Abnormal Heart Rate Recovery after Treadmill Exercise Test in Patients With Coronary Artery Disease

To evaluate the values of abnormal heart rate recovery （HRR） after treadmill exercise test in patients with coronary artery disease （CAD）. Methods One hundred and seventy-eight consecutive cases of suspected CAD who underwent symptom-limited treadmill exercise test （TET） and coronary angiography （CAG） were enrolled and divided into normal and abnormal HRR group based on the status of the values of HRR one or two minutes after TET. The clinical characteristics, TET parameters and CAG results of the two groups were compared attempted to assess the value of HRR on patients with CAD. Results （ 1 ） The cases of smoking, diabetes mellitus （DM） and ST segment deviation at rest in abnormal HRR group were more significantly than those in normal HRR group （ all P 〈 0. 05 ）. （2） The subjects of abnormal HRR usually had higher basal heart rate, more cases exhibited ST segment abnormality and or exercise-limited angina during or after TET（P 〈 0. 01 and P 〈 0. 05, respectively）, but lower level of peak heart rate attained （ P 〈 0. 05 ） than those in normal group. The values of metabolism equivalents and duration of TET between the two groups displayed phenomenal difference （ P 〈 0. 05 ）. There were more samples acquired moderate to high level of Duke test score and chronotropic incompetence in the group of abnormal HRR, compared to the normal HRR group （P 〈 0. 01 ）. （3） The cases of negative CAG results in the group of normal and abnormal HRR group were 73 （66. 97 % ） and 24 （34. 78 % ）. Cases of significant coronary lesions （ at least one major coronary vessel ≥ 50 % stenosis） amongst the subgroup of positive CAG were 36 （ 33.03 % ） and 45 （65.22 % ）, severe coronary lesions （ three-vessel, left main or the equivalents of left main） were 10 （9. 17 % ） and 17 （24. 64 % ） for normal and abnormal HRR respectively （P 〈 0. 01 ）. Accordingly, the Gensini scores in the subunit of abnormal HRR increased. （4）Linear correlation analysis indicate there was a negative correlation between the values of HRR in the first and second minutes and indices of severity of CAD （ all P 〈 0. 01 ）. The analysis of auxiliary diagnostic value of abnormal HRR indicated the annexed HRR standard had higher negative predictive value. Conclusions The status of HRR after TET are not only influenced by the clinical factors related to the cardiac autonomic function, but also associated with the extent of CAD. （ S Chin J Cardiol 2009 ; 10（1）：1-8）