mitochondrial myopathies/hypoxia

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Changes in volume densities and distribution of mitochondria in rat skeletal muscle after chronic hypoxia.

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In order to test the hypothesis that subsarcolemmal aggregation of skeletal muscle mitochondria, as noted in some patients with mitochondrial myopathies, is caused by an impaired oxygen supply to mitochondria, we exposed two groups of rats to 8% O2 during 44 or 45 days. One group performed mild

Increased capillaries in mitochondrial myopathy: implications for the regulation of oxygen delivery.

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Human skeletal muscle respiratory chain defects restrict the ability of working muscle to extract oxygen from blood, and result in a hyperkinetic circulation during exercise in which oxygen delivery is excessive relative to oxygen uptake and oxygen levels within contracting muscle are abnormally

MITOCHONDRIAL MYOPATHY: A NEW THERAPEUTIC APPROACH.

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Restoration of deoxyribonucleic acid in mitochondrial myopathies may occur after a mechanical or chemical injury of striated muscle or by endurance training. Therapies with enzymes, gene therapies, or treatments with substances that stimulate mitochondrial biogenesis are used at the moment. Genesis

Recurrent respiratory insufficiency and depressed ventilatory drive complicating mitochondrial myopathies.

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Three patients with mitochondrial myopathies and progressive external ophthalmoplegia had repeated episodes of respiratory failure requiring assisted ventilation. Studies in these patients and asymptomatic family members, as well as a sporadic case of Kearns-Sayre syndrome, demonstrated markedly

Hypoxic ventilatory depression in a patient with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes.

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We describe a case of a 21-year-old man with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS) who presented with hypoxic ventilatory depression. He had chronic hypoventilation, which was not explained by weakness of respiratory muscles. His hypercapnic

Mitochondrial myopathies and the role of the pathologist in the molecular era.

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Mitochondrial encephalomyopathies are under increasing consideration in the differential diagnosis of diverse metabolic diseases from infancy to late adulthood. This is to be expected considering the vital importance of mitochondria to cellular respiration in all eukaryotes. the vulnerability of the

Influence of erythrocyte oxygenation and intravascular ATP on resting and exercising skeletal muscle blood flow in humans with mitochondrial myopathy.

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Oxygen (O₂) extraction is impaired in exercising skeletal muscle of humans with mutations of mitochondrial DNA (mtDNA), but the muscle hemodynamic response to exercise has never been directly investigated. This study sought to examine the extent to which human skeletal muscle perfusion can increase

An impaired mitochondrial electron transport chain increases retention of the hypoxia imaging agent diacetylbis(4-methylthiosemicarbazonato)copperII.

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Radiolabeled diacetylbis(4-methylthiosemicarbazonato)copper(II) [Cu(II)(atsm)] is an effective positron-emission tomography imaging agent for myocardial ischemia, hypoxic tumors, and brain disorders with regionalized oxidative stress, such as mitochondrial myopathy, encephalopathy, and lactic

[Mechanical ventilation in neuromuscular diseases: do not start too early, but certainly not too late].

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Three patients had chronic respiratory disorders: a 42-year-old man with glycogenosis type II was tired, had headaches, poor pulmonary function values and, according to the arterial blood gas values, hypercapnia; a man aged 24 with Duchenne's muscular dystrophy had variable moderate dyspnoea with

Disruption of mitochondrial respiration inhibits volume-regulated anion channels and provokes neuronal cell swelling.

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Hypoxia and inhibitors of mitochondrial respiration impair the regulatory volume decrease (RVD) of cerebellar granule neurons after hypotonic swelling. RVD is linked to the opening of volume-regulated anion channels (VRACs). VRACs are outwardly rectifying, inactivate slowly during maintained

Radiolabeled Cu-ATSM as a novel indicator of overreduced intracellular state due to mitochondrial dysfunction: studies with mitochondrial DNA-less ρ0 cells and cybrids carrying MELAS mitochondrial DNA mutation.

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OBJECTIVE Radiolabeled Cu-diacetyl-bis (N(4)-methylthiosemicarbazone) (*Cu-ATSM), including (60/62/64)Cu-ATSM, is a potential imaging agent of hypoxic tumors for positron emission tomography (PET). We have reported that *Cu-ATSM is trapped in tumor cells under intracellular overreduced states, e.g.,

Mitochondria and heart failure.

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OBJECTIVE Energetic abnormalities in cardiac and skeletal muscle occur in heart failure and correlate with clinical symptoms and mortality. It is likely that the cellular mechanism leading to energetic failure involves mitochondrial dysfunction. Therefore, it is crucial to elucidate the causes of

Lactic acidosis in childhood.

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Children with chronic metabolic acidosis should be investigated to determine the presence of an organic acid, especially when the plasma electrolyte profile shows a deficiency of anion. One of the organic acids that should be looked for in such a patient is lactic acid. Lactic acidosis due to tissue

Molecular hydrogen as an emerging therapeutic medical gas for neurodegenerative and other diseases.

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Effects of molecular hydrogen on various diseases have been documented for 63 disease models and human diseases in the past four and a half years. Most studies have been performed on rodents including two models of Parkinson's disease and three models of Alzheimer's disease. Prominent effects are

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