Instituto de Investigaciones en Ciencias de la Salud (INICSA)-Cátedra de Física Biomédica, FCM, UNC/CONICET, Córdoba, Argentina.
INCOR, La Rioja, Argentina.
Arch Med Res. 2014 Apr;45(3):237-46. doi: 10.1016/j.arcmed.2014.03.003. Epub 2014 Mar 21.
The fundamental mechanisms involved in the genesis and progression of heart failure are not clearly understood. The present study was conducted to analyze the cardiac mitochondrial involvement in heart failure, the possible parallelism between cardiac and skeletal muscle and if there is a link between clinical symptoms and mitochondrial damage.
Left ventricle and pectoral biopsies were obtained from patients with heart failure (n: 21) and patients with inter-auricular communication as the unique diagnosis for surgery (n: 6). Mitochondria were isolated from these tissues and studied through electron microscopy, spectrophotometry to measure the activity of respiratory complex III and immunohistochemistry to determine the presence of reactive oxygen species.
More than 90% of cardiac and skeletal muscle mitochondria presented structural and functional alterations in relation to an increment in the reactive oxygen species production, even in patients without the presence of any clinical Framingham criteria.
We demonstrated some parallelism between cardiac and skeletal muscle mitochondrial alterations in patients with heart failure and that these alterations begin before the major clinical Framingham criteria are installed, pointing to mitochondria as one of the possibly responsible factors for the evolution of cardiac disease.
心力衰竭发生和发展的基本机制尚不清楚。本研究旨在分析心力衰竭中心肌线粒体的参与情况,以及心肌和骨骼肌之间是否存在平行关系,是否存在临床症状与线粒体损伤之间的联系。
从心力衰竭患者(n=21)和因房间隔缺损而接受手术的患者(n=6)的左心室和胸肌活检组织中分离出线粒体,通过电子显微镜、分光光度法测量呼吸复合物 III 的活性以及免疫组织化学法来检测活性氧物质的存在。
超过 90%的心肌和骨骼肌线粒体存在结构和功能改变,与活性氧物质产生的增加有关,即使在没有任何临床弗雷明汉标准的患者中也是如此。
我们证明了心力衰竭患者心肌和骨骼肌线粒体改变之间存在一些平行关系,这些改变发生在主要的临床弗雷明汉标准出现之前,提示线粒体可能是导致心脏疾病进展的一个可能因素。