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        β腎上腺素能受體在腦心綜合征致心律失常的作用
        來源: | 作者: | 發布時間:2013-11-8 17:14:03

        β腎上腺素能受體在腦心綜合征致心律失常的作用
        趙劍,崔丹,王玲
        基金項目:基金項目:教育部博士點基金(20092307110015);哈爾濱市科技局優秀學科帶頭人基金(2009RFXXS020)
        作者簡介:趙劍,(1988-),男,碩士,主要研究方向:心腦血管疾病
        通信聯系人:王玲,(1960-),女,教授,博士生導師,主要研究方向:心腦血管疾病.

        (哈爾濱醫科大學 生理學教研室,黑龍江 哈爾濱 150081)
        摘要:目的: 探索β腎上腺素能受體在腦心綜合征中致心律失常的機制。 方法: 腦心綜合征模型(MCAO)采用線栓法栓塞大腦中動脈制作。Wistar 雄性大鼠108 只隨機分為正常對照組,腦心綜合征模型組,阿替洛爾組(0.2mg/kg、2mg/kg、20mg/kg),異丙腎上腺素組(0.3mg/kg、0.6mg/kg、1.2mg/kg),維拉帕米組(20mg/kg)。檢測各組心電圖和心肌細胞內鈣濃度的變化。 結果: 大鼠線栓法制作MCAO 模型后88.1%大鼠(16.7±9.5)分鐘出現多種類型的心律失常;0.2mg/kg、2mg/kg、20mg/kg 阿替洛爾給藥后制作MCAO模型,大鼠心律失常概率分別為58.3%,25%和16.7%;而正常大鼠腹腔注射0.3mg/kg、0.6mg/kg1.2mg/kg 異丙腎上腺素,大鼠出現心律失常概率分別為66.7%,83.3%和91.7%,且同種類型心律失常嚴重程度因給藥濃度增加而加重。30μmol/L KCL 處理心肌細胞后,MCAO 模型組和異丙腎上腺素組與對照組相比心肌細胞內鈣濃度顯著升高(p<0.01)。阿替
        洛爾組、維拉帕米組與MCAO 模型組相比心肌細胞內鈣濃度顯著降低(p<0.01)。 結論:腦心綜合征中腎上腺素通過激動β1 受體參與心律失常的發生和心肌細胞內鈣濃度的改變。
        關鍵詞:腦心綜合征;β1腎上腺素能受體;阿替洛爾;心律失常;異丙腎上腺素
        中圖分類號:R5
        The effect of β adrenergic receptor on arrhythmia in cerebrocardiac syndrome
        ZHAO Jian, CUI Dan, WANG Ling
        (Department of Physiology,Harbin Medical Unversity,Heilongjiang,Harbin 150081)
        Abstract: Objective : To explore the role of beta adrenergic receptor in arrhythmia in cerebrocardiac syndrome(CCS). Methods: The MCAO models were made by thread embolism method. 108 wistar male rats were randomly divided into normal group,MCAO model group,atenolol group(0.2mg/kg,2mg/kg,20mg/kg),isoprenaline(ISO)group(0.3mg/kg,0.6mg/kg,1.2mg/kg)and verapamil group(20mg/kg),then detect the electrocardiogram and myocardial intracellular calcium concentration of each group. Results: 88.1% MCAO rats showed various types of arrhythmia within 16.7±9.5 minutes; The arrhythmia rate in 0.2mg/kg, 2mg/kg and 20mg/kg atenolol group were 58.3%, 25% and 16.7% respectively; While the 0.3 mg/kg, 0.6mg/kg,1.2mg/kg ISO group were 66.7%, 83.3% and 91.7% respectively. The myocardial intracellular calcium concentration in MCAO group and ISO group significantly increased compared with the control group after 30μmol/L KCL treatment (p<0.01). The myocardial intracellular calcium concentration in atenolol group and verapamil group decreased significantly compared with the MCAO group after 30μmol/L KCL treatment (p<0.01). Conclusion: The intracellular calcium concentration increasing and arrhythmia happened in CCS were caused by the the activating of β 1receptor.
        Key words: cerebro-cardiac syndrome; β1-adrenergic receptor; arrhythmia; isoprenaline;atenolol

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