临时起搏在非心脏手术中的应用分析

目的:探讨临时起搏器在非心脏手术中常合并有心脏起搏及传导系统的功能障碍应用的必要性。方法:对60例合并缓慢型心律失常的外科患者在手术前1天或术前4h植入心脏临时起搏器,术中和术后行心电图监测记录,观察起搏器的工作状态。结果:60例中起搏器起搏有71.67%,其中严重窦性心动过缓、Ⅱ度AVB、房颤伴长间歇(>2s)和双束支阻滞的患者临时起搏器工作状态多,患者合并心肌梗死和心肌病时,是术中发生严重缓慢性心律失常的高危人群,具有临时起搏器植入的明显指征。结论:在非心脏手术中合并有缓慢型心律失常、Ⅱ度AVB、房颤伴R-R长间歇和双束支阻滞者在行外科手术前植入心脏临时起搏器可以为手术的顺利进行提供安全保障。     

车祸伤并不典型主动脉夹层1例

患者,女,69岁,因"反复胸痛10余天"入院。于10余天前因车祸撞击胸部后反复出现胸痛,为胸骨后隐痛,无腹痛、背痛及肩背部放射痛,无汗。在当地医院就诊,胸片提示肋骨骨折,予对症治疗;     

不典型缩窄性心包炎误诊为冠心病1例

患者,女,39岁,因发作性胸闷胸痛10余年,加重3 d,晕厥1次于2010年7月10日入院.10余年前开始反复于劳累后发作胸闷胸痛,每次发作持续几分钟,无肩背部放射痛,无气促,休息后可自行缓解,未予重视;3 d前患者无明显诱因突发剧烈胸闷,伴气促及背部疼痛,继而出现意识丧失,约10 min左右神志自行恢复,到当地医院就诊,测血压70/40 mmHg,作心电图提示窦性心律,心率90次/min,Ⅱ、Ⅲ、avF、V1～V3导联ST段下移0.05～0.1 mV,给予多巴胺升压及对症处理后约30 min患者A:X线片;B:CT图1 心包钙化及增厚的影像学检查胸闷等症状缓解;在当地医院住院期间患者仍反复发作胸闷、胸痛,查胸片及心脏彩超未见异常(仅见报告单),为进一步诊治转入我院.     

青钱柳叶对糖尿病大鼠血糖、血脂和抗氧化作用的影响

目的观察青钱柳叶对糖尿病大鼠血糖、血脂和抗氧化作用的影响。方法将50只SPF级Wistar大鼠随机分为空白对照组、模型对照组、青钱柳叶低、中、高剂量组,模型组在高热能饲料喂养基础上给予地塞米松0.8mg/kg腹腔注射造模,青钱柳叶低、中、高剂量组分别给予0.06g/(kg·d)、0.3g/(kg·d)、0.6g/(kg·d)剂量灌胃,检测血糖、糖化血红蛋白、甘油三酯、总胆固醇、丙二醛、超氧化物歧化酶。结果与空白对照组比较,模型组血糖、糖化血红蛋白、甘油三酯、总胆固醇、丙二醛明显升高,超氧化物歧化酶明显降低,差异具有统计学意义(P0.01);与模型组比较,中剂量组、高剂量组血糖、糖化血红蛋白、甘油三酯、总胆固醇、丙二醛明显降低,超氧化物歧化酶明显升高,差异具有统计学意义(P0.05),随剂量增加,降低趋势明显,但中剂量组和高剂量组无显著性差异(P0.05)。结论青钱柳叶可有效降低2型糖尿病大鼠血糖、血脂,保护机体免受自由基伤害,且不良反应较少,安全性高,值得临床推广。     

原发性高血压患者血清C反应蛋白与血压的相关性研究

C反应蛋白（C—reactive protein,CRP）发现至今已有60余年的历史。近年来对其生物合成、结构、理化性质、生物学特性、检测方法及临床应用等方面进行了广泛深入的研究。CRP不仅可以作为急性炎症诊断指标之一,而且在高血压等心脑血管疾病、代谢性疾病、肾脏疾病、肝脏疾病、胰脏疾病等疾病中存在慢性炎症,持续CRP升高对该疾病的发现、诊断、治疗和预后具有一定的临床价值。     

右室流出道室性早搏患者的窦性心率震荡变化

目的观察右室流出道室性早搏患者窦性心率震荡（HRT）的变化并探讨其临床意义。方法52例右室流出道室性早搏患者按室早数目分为两组：A组（室早≥1000／24h）和B组（室早〈1000/24h），比较两组间的HRT参数震荡初始（TO）和震荡斜率（TS）。结果右室流出道室性早搏患者HRT异常的发生率为23．08％，且A组患者中异常HRT的发生率明显高于B组；与B组相比，A组患者的TO值明显增大，幅值降低（p均〈0．05）；HRT与室早数目呈明显正相关（p〈0．01），TS与室早数目呈明显负相关（p〈0．01）。结论频发右室流出道室性早搏（室早≥1000／24h）患者的窦性心率震荡现象减弱，且HRT与室性早搏数目明显相关。HRT是一种较好的检测心脏自主神经功能的新技术。     

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.     

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.     

复方丹七胶囊对动脉粥样硬化家兔血脂及内皮细胞功能的影响

目的探讨复方丹七胶囊对动脉粥样硬化（AS）家兔血脂的调节作用及对内皮细胞功能的影响。方法动物随机分成模型组、复方丹参组、复方丹七胶囊小剂量组、中剂量组、大剂量组，正常组。正常组予基础饲料喂养，其余5组均高脂饲料喂养。2周后给药保护4周。复方丹参组给予复方丹参片。每2．5h体重1片，复方丹七胶囊大、中、小剂量组分别给予复方丹七胶囊（相当于生药0．3g／kg、0．9g／kg、2．7g／kg）。结果复方丹七胶囊能调节AS家兔血脂，降低血清中升高的总胆固醇（TC）、三酰甘油（TG）、低密度脂蛋白（LDL—C）、ApoB水平，升高高密度脂蛋白（HDL—C）、ApoAl含量，能调节HDL—C／LDLC、ApoAl／ApoB的比值．具有明显的剂量相关性；同时能提高血中一氧化氮（NO）含量，降低血浆内皮素-1的含量，调节、恢复两者之间的相对平衡。结论复方丹七胶囊具有调节血脂和保护内皮细胞功能的作用。     

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.