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Aim: QT interval prolongation can result from intake of drugs known to affect the rapidly activating delayed rectifier K+ channel (IKr) encoded by human ethera-go-go-related gene (hERG).We aimed to investigate the pathophysiological consequences of a non-sense mutation, Q738X, in hERG and the effects of propofol on reconstituted wild type (WT) and Q738X hERG currents.