Dietary inorganic nitrate alleviates doxorubicin cardiotoxicity: mechanisms and implications. (73/115)

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Effects of mechanical over-loading on the properties of soleus muscle fibers, with or without damage, in wild type and mdx mice. (74/115)

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Mouse gastrocnemius muscle regeneration after mechanical or cardiotoxin injury. (75/115)

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microRNA-206 promotes skeletal muscle regeneration and delays progression of Duchenne muscular dystrophy in mice. (76/115)

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Desferrioxamine attenuates doxorubicin-induced acute cardiotoxicity through TFG-beta/Smad p53 pathway in rat model. (77/115)

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Loss of STAT1 in bone marrow-derived cells accelerates skeletal muscle regeneration. (78/115)

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Cardiotoxic local anesthetics increasingly interact with biomimetic membranes under ischemia-like acidic conditions. (79/115)

The cardiotoxic effects of local anesthetics increase in cardiac ischemia which is characterized by the tissue pH lowering to 6.5 or less. Apart from the cardiac channel blockade, the membrane interaction has been referred to as another mode of their cardiotoxic action. By using biomimetic membranes, we verified the hypothesis that bupivacaine and lidocaine may increasingly interact with cardiac mitochondrial membranes under ischemia-like acidic conditions. Biomimetic membranes were prepared with different phospholipids and cholesterol to be unilamellar vesicles suspended in buffers of pH 7.4, 6.9, 6.4 or 5.9. Bupivacaine and lidocaine were reacted with the membrane preparations at cardiotoxically relevant concentrations and their membrane interactivities were determined by measuring fluorescence polarization. Both drugs interacted with 100 mol% 1,2-dipalmitoylphosphatidylcholine, peripheral nerve cell-mimetic and cardiomyocyte-mimetic membranes to increase membrane fluidity, although lowering the reaction pH from 7.4 to 5.9 decreased their membrane-fluidizing effects. In cardiomyocyte mitochondria-mimetic membranes containing 20 mol% cardiolipin, however, bupivacaine and lidocaine reversely increased their membrane interactivities at pH 5.9-6.4 compared with pH 7.4. Such increases were greater in anionic phospholipid membranes which consisted of substantial amounts of cardiolipin and phosphatidylserine. Positively charged bupivacaine and lidocaine would form ion-pairs with the negatively charged head-groups of anionic phospholipids under acidic conditions, thereby increasing the induced membrane fluidization. The mitochondrial membrane interactions depending on pH lowering may be, at least in part, responsible for local anesthetic cardiotoxicity enhanced in acidosis associated with cardiac ischemia.  (+info)

Sodium nitroprusside induces cell death and cytoskeleton degradation in adult rat cardiomyocytes in vitro: implications for anthracycline-induced cardiotoxicity. (80/115)

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