| 赵京林,杨跃进,尤士杰,荆志成,吴永建,杨伟宪,陈纪林,高润霖,陈在嘉.通心络对猪急性心肌梗死再灌注后内皮素-1的影响[J].,2005,(10):902-906 |
| 通心络对猪急性心肌梗死再灌注后内皮素-1的影响 |
| Effect of Tongxinluo on Endothelin-1 in the Mini-Swine Model of Acute Myocardial Infarction and Reperfusion |
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| DOI： |
| 中文关键词: 通心络 内皮素-1 无再流 急性心肌梗死 猪 |
| 英文关键词:Tongxinluo endothelin-1 no-reflow acute myocardial infarction swine |
| 基金项目:国家自然科学基金资助项目(No.90209038) |
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| 中文摘要: |
| 目的评价急性心肌梗死(acute myocardial infarction,AMI)再灌注后内皮素-1(endothelin-1,ET-1)的变化及通心络对其影响,探讨无再流的可能机制。方法中华小型猪40只,随机分成模型组,小、中和大剂量通心络治疗组和假手术组,每组8只。冠状动脉结扎3h,松解1h制备AMI再灌注模型。采用放射免疫方法(RIA)测定造模前、后和再灌注后血清及AMI再灌注后心肌组织ET-1含量;逆转录-聚合酶链反应(RT-PCR)的方法观察正常、缺血和无再流区心肌组织ET-1mRNA的表达。结果(1)与造模前比较,模型组造模后5min时、造模后3h、再灌注5min和1h的血ET-1水平显著升高,且呈递增趋势(均P<0·01)。而ET-1升高幅度中、大剂量通心络组均低于模型组(P<0·05,P<0·01)。(2)与正常区心肌组织比较,模型组和3个通心络组一样,缺血区和无再流区心肌组织中ET-1含量均显著升高(均P<0·01),且无再流区ET-1含量升高比缺血区更显著(均P<0·01)。与模型组比较,中和大剂量通心络组仅缺血区心肌组织中ET-1含量显著降低(P<0·01)。(3)与正常区心肌组织比较,模型组和通心络各组缺血区心肌组织中ET-1mRNA表达均显著上调(均P<0·01),而无再流区心肌组织ET-1mRNA表达均显著下降(均P<0·01)。与模型组比较,中和大剂量通心络组仅缺血区ET-1mRNA表达上调幅度显著降低(P<0·01)。结论内皮细胞受损可能是无再流发生的重要机制之一,通心络可能通过保护内皮细胞起到了减少无再流的作用。 |
| 英文摘要: |
| ObjectiveTo evaluate the change of endothelin-1 (ET-1) in the mini-swine model of acute myocardial infarction (AMI) and reperfusion and the effect of Tongxinluo (TXL) on it, and to explore the possible mechanism of no-reflow. MethodsForty mini-swines were randomized into 5 groups: the model group, the small,middle and large dose of TXL groups and the sham-operated group, 8 in each group. The AMI reperfusion model was established by coronary ligation for 3 hrs followed with relaxation for 1 hr. Plasma ET-1 content before and after AMI, and after reperfusion was determined respectively by radioimmunoassay. The ET-1 mRNA expression in myocardial tissue of normal, ischemic and no-reflow area were respectively quantified by reverse transcription-polymerase chain reaction. Results(1) Compared with before AMI, levels of plasma ET-1 at the time points of 5 min and 3 hrs after AMI, 5 min and 1 hrs after reperfusion in the model group were significantly raised, showing an increasing tendency (all P<0.01). But the increment in the middle and large dose of TXL groups were all lower than that in the model group (P<0.05). (2) In the model and the TXL groups, levels of ET-1 in myocardial tissue of ischemic and no-reflow area were significantly higher than those in the normal area, and the increment in no-reflow area was higher than that in ischemic area (all P<0.01). Compared with the model group, significant lowering of ET-1 in ischemic area was only shown in the middle and large dose of TXL groups (P<0.01). (3) In the model and the TXL groups, ET-1 mRNA expression in ischemic area was significantly higher (all P<0.01), while it in no-reflow area was significantly lower than that in the normal area respectively (all P<0.01). The raised ET-1 mRNA expression in the middle and large dose TXL groups was significantly lowered when compared with that in the model group (P<0.01). Conclusion The endothelium injury might be one of the important mechanisms for no-reflow phenomenon. TXL might reduce the no-reflow by protecting endothelium cells. |
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