Crotonaldehyde inhibits myocardial contractile function in mice / 基础医学与临床

ABSTRACT

Objective To study the effect of an essential α,β-unsaturated aldehyde from cigarette smoke crotonal-dehyde on myocardial contractile function and intracellular Ca2+function in mice. Methods Hearts of from male C57BL/6 mice were digested by Langendorff to islate the cardiomyocytes. The cardiomyocytes of mice were then in-cubated with crotonaldehyde(1,10,25 and 50 μmol/L) for 6 h,and the control group was treated without croton-aldehyde,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),intracel-lular Ca2+decay and SERCA 45Ca2+uptake and the expression of Na+-Ca2+exchange were evaluated by 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,&Delta;FFI,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+exchange in cardiomyocytes. Conclusions Crotonaldehyde may inhibit cardiomyocyte contraction by suppressing SERCA activity and compromising intracellular Ca2+handling.