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BACKGROUND: Epidemiological evidence suggests that a majority of deaths attributed to secondhand smoke (SHS) exposure are cardiovascular related. However, to our knowledge, the impact of SHS on cardiac electrophysiology, Ca2+ handling, and arrhythmia risk has not been studied.

OBJECTIVES: The purpose of this study was to investigate the impact of an environmentally relevant concentration of SHS on cardiac electrophysiology and indicators of arrhythmia.

METHODS: Male C57BL/6 mice were exposed to SHS [total suspended particles (THS): 3.0 +/- 0.1 mg/m(3), nicotine: 0.4 +/- 0.2 mg/m(3), carbon monoxide: 12.4 +/- 1.6 ppm, or filtered air (FA) for 4, 8, or 12 wk (n =4-5/group]. Hearts were excised and Langendorff perfused for dual optical mapping with voltage- and Ca2+-sensitive dyes.

RESULT: At slow pacing rates, SHS exposure did not alter baseline electrophysiological parameters. With increasing pacing frequency, action potential duration (APD), and intracellular Ca(2+)alternans magnitude progressively increased in all groups. At 4 and 8 wk, there were no statistical differences in APD or Ca2+ alternans magnitude between SHS and FA groups. At 12 wk, both APD and Ca2+ alternans magnitude were significantly increased in the SHS compared to FA group (p < 0.05). SHS exposure did not impact the time constant of Ca2+ transient decay (t) at any exposure time point. At 12 wk exposure, the recovery of Ca2+ transient amplitude with premature stimuli was slightly (but nonsignificantly) delayed in SHS compared to FA hearts, suggesting that Ca2+ release via ryanodine receptors may be impaired.

CONCLUSIONS: In male mice, chronic exposure to SHS at levels relevant to social situations in humans increased their susceptibility to cardiac alternans, a known precursor to ventricular arrhythmia.