Estructura de las mitocondrias en miocardio con insuficiencia cardíaca.

GUZMÁN MENTESANA GUSTAVO; BÁEZ ALEJANDRA; CÓRDOBA ROQUE; LO PRESTI SILVINA; RIVAROLA WALTER; PONS PATRICIA; FRETES RICARDO; PAGLINI PATRICIA

UNLaR Ciencia

Revista Científica de la Universidad Nacional de La Rioja

Lugar: La Rioja; Año: 2007 p. 7 - 12

The compression of the mechanisms that lead to heart failure, is one of the greatest challenges of the current cardiology, interpreting the neuro-hormonal mechanisms and how they interact at genetic and molecular level. The heart is an organ with high energy consumption. This vital resource is provided by mitochondria, which represent approximately 30% of the total volume of cardiomyocytes and provide 90% of energy required . Such oxidative activity makes it target of reactive oxygen species (ROS). The energy producted by mitochondria is dependent on gene mythcondriales factors that modulate the normal functioning of the enzyme activities of the organelle (Anderson et al 1987; Shadel & Clayton 1997), as well as environmental factors such as providing substrates carbohydrates, lipids, proteins and oxygen for the formation of energy (Marin-Garcia & Goldenthal 2002). These pathways are identified as crucial points for oxidation of fatty acids and the final route of the common  pyruvate oxidation, oxidative phosphorylation, which generates 80 to 90% of cellular ATP (Brown et al 1995). The oxidative phosphorylation (OXPHOS) is established through a protein complex located in the internal membrane of mitochondria. These include, the respiratory complex I to IV, ATP synthase (complex V) and the adenine nucleotide transport; being the tracks of fatty acid oxidation and carbohydrate (via tricarboxylic acid) the main sources of electrons for the respiratory chain through the formation of mitochondrial NADH and FADH (Lopaschuck et al 1992). Abnormalities in mitochondrial structure and function in various cardiomyopathies (Garg et al 2005; Marin-Garcia & Goldenthal 2002); some hypertrophy and dilated miocardiopatias have already been identified in the respiratory chain defects in oxidative phosphorylation (Rustin and col 1994; Arbustini et al 1998), as well as mutations in the cytochrome c and deletions of mitochondrial DNA, whose relationship with heart disease has not yet been explained (Schon et al 1997; Arbustini et al 1998; Marin-Garcia et al 2000); defects driving and arrhythmias. In some patients it has been that detected important alterations in the oxidative emphasize is that mitochondria whick target of proinflammatory mediators and other noxas of endogenous and exogenous origin (Garg 2005), which with some ambiguity can behave as growth and simultaneously proapoptotico. On the other hand it has been postulated that the mitochondrial alterations in the heart muscle would be accompanied by similar damages in the same organelle of skeletal muscle (Marin Garcia et al 1999). The aim of this research was to study the changes in the structure of mitochondria of heart and skeletal muscle in congestive heart failure patients with level III-IV arising from míocardiopathy isquemias and valvulopathies to find a correlation between alterations of mitochondria ventricle and skeletal muscle (Tsutsui H 2001), which could allow to know the state of myocardium cells using any striated muscle biopsy.