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Adrenergic stimulation can increase myocardial oxygen consumption, lead to the downregulation of -adrenergic receptors, and reverse adrenergic G protein coupling, resulting in impaired myocardial contractility and septic cardiomyopathy, particularly during prolonged administration [31, 32]

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6b) is more efficient than the formation of the transition state between the glutathionylated enzyme and GSH (Fig

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