Effects of Acetaldehyde on the Isolated Papillary Muscle of Diabetic Rats

Short‐Term Acetaldehyde Exposure Depresses Ventricular Myocyte Contraction: Role of Cytochrome P450 Oxidase, Xanthine Oxidase, and Lipid Peroxidation

“…However, the disparate effect between myocyte shortening (PS) and an intracellular Ca 2ϩ increase (⌬FFI) in response to ACA exposure indicates the possible involvement of a Ca 2ϩ -indpendent mechanism in the ACAinduced cardiac response; this is supported by earlier observations (Figueredo et al, 1998). It is noteworthy that a significant inhibition of cell shortening was achieved at 10 and 50 M ACA but not at 100 M. Although the mechanism of action responsible for this disparity is not known, offsetting effects between the ACA-induced positive ␤-adrenergic cardiac response (Savage et al, 1995) and the direct cardiac depressive action of ACA (Ren et al, 1997) may be speculated. Nevertheless, the offsetting effects did not affect all mechanical indices equally, because 100 M ACA did inhibit the maximal velocity of shortening and relengthening (ϮdL/dt).…”

Ethanol and Hormesis

“…However, the high concentration (> 3 mM) ACA-induced depression of myocardial contraction at both tissue and myocyte levels reduces intracellular Ca 2+ mobilization and inhibits contraction through voltage-dependent channels. According to Brown et al (1999), these collective effects led to the observed negative chronotropic and inotropic effects on myocardial tissues (Savage et al, 1995;Morales et al, 1997;Ren et al, 1997). These findings have been extended by Brown et al (1999) with both normal and hypertensive adult male rats.…”

“…Over the past two decades various researchers have reported that acetaldehyde (ACA) affects biphasic chronotropic and inotropic effects on whole heart and various myocardial tissue preparations, in vitro (Williams et al, 1980;Stratton et al, 1981;Brown and Carpentier, 1989;Savage et al, 1995).…”

ALDH2 in alcoholic heart diseases: Molecular mechanism and clinical implications

“…Acetaldehyde may trigger cardiac hypertrophy or dilated cardiomyopathy associated with a significant increase in the hypertrophic marker skeletal actin and ANF (Li & Ren, 2008; Liang et al, 1999). Direct effects of acute (5 to 10 min) acetaldehyde exposure on cardiovascular function have been extensively studied (Aberle & Ren, 2003; Aistrup et al, 2006; Brown et al, 1999, 2001; Brown & Savage 1996; Ren et al, 1997; Savage et al, 1995). Acetaldehyde produces vasoconstriction and positive inotropic and chronotropic responses at concentrations of 3 mM or below.…”

“…Higher concentrations of acetaldehyde (>3 mM) elicit cardiac depression, vasodilatation and hypotension (Brown & Carpentier, 1989, 1990). The acetaldehyde-induced negative inotropic response in the heart seems to be associated with decreased SR Ca 2+ release (Ren et al, 1997; Savage et al, 1995) or inhibition of voltage-dependent Ca 2+ channels (Morales et al, 1997). Our earlier studies revealed that acetaldehyde depresses cardiomyocyte contractile amplitude, maximal velocity of contraction/relaxation, and prolonged duration of relaxation and intracellular Ca 2+ clearance (Aberle et al, 2004; Aberle & Ren, 2003; Ren et al, 1997).…”