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Ischemia/reperfusion injury in male guinea pigs: An efficient model to investigate myocardial damage in cardiovascular complications

机译:雄性豚鼠的缺血/再灌注损伤:一种有效的模型,用于探讨心血管并发症心肌损伤的高效模型

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Myocardial ischemia/reperfusion (I/R) injury is the major problem that aggravates cardiac damage. Several established animal models fail to explain the similarity in disease mechanism and progression as seen in humans; whereas guinea pig shows high similarity in cardiovascular parameters. Hence, current study is aimed to develop an animal model using guinea pigs that may best correlate with disease mechanism of human myocardial I/R injury. Male guinea pigs were randomized into three groups: normal diet (ND), high fat diet (HFD) and sham; fed with respective diets for 90 days. Myocardial infarction (MI) was induced by ligating left anterior descending artery (LAD) for 30 min followed by 24 h and 7 days of reperfusion in ND and HFD groups. Electrocardiogram (ECG) showed the alterations in electrical conduction during myocardial I/R injury. Elevated levels of lactate dehydrogenase (LDH) and creatine kinase-MB ((CK-MB)) were higher in HFD compared to ND. Inflammatory markers such as tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) were up-regulated in I/R injury animals compared to sham. Fold change of these protein expression levels were higher in HFD compared to ND. Elevated lipid profile and increased aortic wall thickness in HFD animals depicts the risk of developing cardiovascular complications. ECG analysis strongly confirmed MI through changes in sinus rhythm that are reflected in infarcted tissue as verified through TTC staining. Thus the combination of HFD followed by I/R injury proved to be an efficient model to study pathophysiology of myocardial I/R injury with minimal tissue damage and surgical mortality.
机译:心肌缺血/再灌注(I / R)损伤是加重心脏损伤的主要问题。几种已建立的动物模型未能解释人类中所见的疾病机制和进展中的相似性;虽然豚鼠在心血管参数中显示出高相似性。因此,目前的研究旨在使用可能与人心肌I / R损伤的疾病机制最佳相关的豚鼠来开发动物模型。雄性豚鼠随机分为三组:正常饮食(ND),高脂饮食(HFD)和假;喂食各种饮食90天。通过连接左前后下降动脉(LAD)诱导心肌梗死(MI)30分钟,然后在Nd和HFD基团中再灌注24小时和7天。心电图(ECG)显示心肌I / R损伤期间导电的改变。与Nd相比,HFD升高的乳酸脱氢酶(LDH)和肌酸激酶-MB((CK-MB))较高。与假的I / R损伤动物相比,炎症标记如肿瘤坏死因子-α和白细胞介素-6(IL-6)上调。与Nd相比,HFD的这些蛋白质表达水平的折叠变化较高。高脂质曲线和HFD动物中的主动脉壁厚度提高,描绘了发育心血管并发症的风险。 ECG分析通过鼻窦节律的变化强烈证实了MI,其在通过TTC染色验证的梗死组织中反映。因此,HFD的组合随后I / R损伤被证明是一种有效的模型,用于研究心肌I / R损伤的病理生理学,具有最小的组织损伤和外科死亡率。

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