Whether alcohol-induced heart failure is caused by a direct toxic effect of
ethanol, metabolites, or whether it is a secondary result of neurohumoral,
hormonal, or nutritional factors is not clear, To address this question a
Langendorff retrograde coronary perfusion model of rat heart was used to st
udy the effect of 0.5% (v/v) ethanol (n = 7) and 0.5 mM acetaldehyde (n = 9
) on left ventricular expression of ANP, BNP, p53, p21, TNF-alpha, bax, bcl
-2 as well as on DNA-fragmentation. Ethanol infusion of 150 min duration si
gnificantly induced both ANP and p21 mRNA expression of ventricular myocard
ium compared with hearts infused with vehicle (n = 8), Acetaldehyde did not
exert any significant effects on any of the parameters studied, although t
he mean expression of TNF-alpha tended to be lower in the acetaldehyde-trea
ted hearts than in control hearts. No evidence of increased DNA-fragmentati
on was found in ethanol or acetaldehyde treated groups. We conclude that et
hanol per se is capable of inducing genes associated with hypertrophy and i
mpaired function of the heart whereas a significant apoptosis is not involv
ed in the initial phase of alcohol-induced cardiac injury. (C) 2001 Academi
c Press.