肾上腺素能受体阻滞剂对心肌梗死后心肌局部α1受体密度及电生理稳定性的影响  

Effects of Adrenergic Receptor Anagonist on Myocardial α_1-AR Density and Cardiac Electrophysiological Stability in Rabbits After Myocardial Infarction

作　　者：张静敏[1] 伍卫[1] 方昶[1] 张燕[1] 王景峰[1] 

机构地区：[1]中山大学附属第二医院心内科,广东广州510120

出　　处：《中山大学学报（医学科学版）》2003年第6期552-555,共4页Journal of Sun Yat-Sen University:Medical Sciences

基　　金：广东省教育厅"千百十工程"优秀人才培养基金项目(Q02032)

摘　　要：【目的】观察β受体(β-AR)阻滞剂(美托洛尔)及α1受体(α1-AR)阻滞剂(哌唑嗪)对急性心肌梗死后心室肌α1-AR密度变化及心室有效不应期离散度(VERP-D)的影响。【方法】健康成年雄性新西兰兔24只,随机分成4组,每组各6只:正常对照组、安慰剂组、美托洛尔组、哌唑嗪组。建立急性心肌梗死模型,自术后第1天起,各组分别予相应药物口服,疗程7d。疗程结束后再次开胸,用S1S2负向扫描法测定VERP-D,然后取心室肌组织,检测心室正常区、缺血区α1-AR、以及β-AR密度。【结果】①心肌梗死后安慰剂组心室肌缺血区和正常区的α1-AR及β-AR均上调(P<0.01);②美托洛尔组上述区域α1-AR及β-AR仍上调(P<0.01),但在正常区α1-AR上调幅度大于安慰剂组(P<0.01),β-AR上调幅度则缩小(P<0.05);③哌唑嗪组上述区域α1-AR下调(P<0.01),β-AR虽上调,但与安慰剂组比较上调幅度无明显变化(P>0.05);④心肌梗死后心室肌组织VERP-D增大(P<0.01),口服美托洛尔或哌唑嗪均可使VERP-D增大的幅度缩小(P<0.01),但两者之间的差别无统计学意义(P>0.05)。【结论】心肌梗死后心室肌组织α1-AR活性增强;缺血状态下应用β受体阻滞剂可能会使心肌α1-AR功能进一步亢进,参与心肌梗死后一系列病理生理过程;To investigate the effects of adrenergic receptor(AR) anagonist ( metoprolol and prazosin) on myocardialα1 AR density and the changes of ventricular effective refractory period depersion(VERP D)in rabbits after myocardial infarction(MI). Twenty four adult male New Zealand rabbits were divided into four groups at random: the control group (n=6); the MI with placebo group (n=6); the MI with metoprolol group (n=6) ; the MI with prazosin group (n=6). The rabbits received drugs for seven days, beginning at the first day after MI with metoprolol 5 mg·kg-1·d-1 or prazosin 0.2 mg·kg-1·d -1. On the seventh day after MI, chests of these rabbits were reopened.VERP D and the density of myocardial α1 AR andβ AR density were measured.①In the placebo group,on the seventh day after MI , the density of ventricularα1 AR and β AR were both increased in comparison with control group( P< 0.01). ②In the metoprolol group, on the seventh day after MI , the density of ventricularα1 AR and β AR were still increased in comparison with control group( P< 0.01). But in comparison with placebo group, the density of ventricular α1 AR in normal region in the metoprolol group was increased(P< 0.01),while the density of β AR was decreased(P< 0.05).③In the prazosin group, on the seventh day after MI , the density of ventricularα1 AR was decreased in comparison with control group( P< 0.01). The changes of β AR had no significance in comparison with control group(P >0.05).④VERP D was increased after MI(P< 0.01). After metoprolol or prazosin treatment ,VERP D was decreased (P< 0.01). [Conclusion]After acute MI,α1 AR of ventricular myocardial was upregulated, which may be accompanied by its activitation. When treated with metoprolol after MI, the density of myocardialα1 AR became upregulated more greatly. When treated with metoprolol or prazosin, cardiac electrophysiological stability may be improved obviously.

关 键 词：肾上腺素能受体阻滞剂 心肌梗死 心肌 α1受体密度 电生理 稳定性 

分 类 号：R542.22[医药卫生—心血管疾病]