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carboxyatractyloside/hypoxia

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7 結果
Hypoxia and reoxygenation in working rat hearts were investigated in this study. Cardiac hemodynamic parameters which decline immediately under hypoxic conditions, recover during reoxygenation. Biochemical and ultrastructural alterations exhibit a more complicated pattern. There is a primary phase
The purpose of the present study was to explore the effects of hypoxic exposure on mitochondrial adenine nucleotide translocator (ANT) activity and its characteristics. Male Wistar rats were exposed to hypoxia in a hypobaric chamber simulating high altitude at 5 000 m for 1, 5, 15 and 30 d. Control
To assess the direct renal toxicity of carboxyatractyloside (CATR), it was administered in relatively low intravenous (i.v.) doses (6.5 and 13.0 mumol/kg) to pentobarbital-anesthetized dogs that were being mechanically ventilated in order to circumvent severe extrarenal effects, such as hypoxemia,
Kidney proximal tubules develop a severe but highly reversible energetic deficit due to nonesterified fatty acid (NEFA)-induced dissipation of mitochondrial membrane potential (DeltaPsi(m)) during reoxygenation after severe hypoxia. To assess the mechanism for this behavior, we have compared the
The influence of mitochondrial function on intracellular signalling is currently under intense investigation. In this regard, we analysed the effect of adenine nucleotide translocase 1 (ANT1), which facilitates the exchange of ADP and ATP across the mitochondrial membrane, on cell-protective
The cardioprotective concentration range of the thiol drug 2-mercaptopropionylglycine (MPG) was investigated during reoxygenation after 30 min of hypoxia. It was found that aortic flow and frequency were increased by 1 mM MPG. Coronary flow, systolic and diastolic pressure were not significantly

Protective role of adenine nucleotide translocase in O2-deficient hearts.

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At subsaturating concentrations of palmitoyl-CoA, the carnitine-dependent oxidation of the palmitoyl portion by uncoupled rat heart mitochondria was stimulated by ADP or ATP. This effect was traced to the prevention of acyl-CoA binding to adenine nucleotide translocase and the consequent sparing of
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