Abstract: Objective To study the effect of an essential α,β-unsaturated aldehyde from cigarette smoke crotonaldehyde on myocardial contractile function and intracellular Ca2+ function in mouse. Methods Hearts were removed from male C57BL/6 mice were digested by Langendorff to islate the cardiomyocytes. The cardiomyocytes of mice were then incubated with crotonaldehyde (1, 10, 25 and 50 μmol/L) for 6 h, and the control group was treated without crotonaldehyde, then they were evaluated including peak shortening (PS), maximal velocity of shortening/relengthening (±dL/dt), time-to-PS (TPS), time-to-90% relengthening (TR90), fura-2 fluorescence intensity (FFI), intracellular Ca2+decay and SERCA 45Ca2+ uptake and the expression of Na+-Ca2+ exchanger were evaluated using Western blot analysis. Results Compared with the control group, the higher concentrations of the crotonaldehyde(25 and 50 μmol/L) groups significantly diminished the PS, ±dL/dt, ΔFFI, SERCA activity and Ca2+ decay (P<0.05), as well as prolonged the TR90 (P<0.05); however the crotonaldehyde with different concentrations had no effect on the expression of Na+-Ca2+ exchanger in cardiomyocytes. Conclusions Crotonaldehyde may inhibit cardiomyocyte contraction by suppressing SERCA activity and compromising intracellular Ca2+ handling.

Key words: Keywords: Crotonaldehyde, Cardiomyocytes, Contractile function, SERCA