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Aldehyde Dehydrogenase Inhibition Ameliorates Cardiac Dysfunction and Exacerbates Hypotension Caused by Alcohol in Female Rats.

BACKGROUND
Aldehyde dehydrogenase 2 (ALDH2) protects against alcohol-evoked cardiac dysfunction in male rodents but its role in the estrogen (E2 )-dependent hypersensitivity of female rats to alcohol-evoked myocardial oxidative stress and dysfunction is not known.


STUDY DESIGN
We addressed this question by studying the effect of cyanamide (ALDH2 inhibitor) on cardiac function, blood pressure, alcohol metabolizing enzymes (alcohol dehydrogenase, cytochrome P450 2E1, catalase and ALDH2) activities and cardiac redox status (reactive oxygen species, ROS; malondialdehyde, MDA) in the absence or presence of ethanol in female sham-operated (SO) and ovariectomized (OVX) rats.


RESULTS
Cyanamide attenuated the ethanol-evoked myocardial dysfunction (reduced dP/dtmax and LVDP) in SO rats. Ethanol, cyanamide or their combination did not alter dP/dtmax or LVDP in OVX rats. Cyanamide induced cardiac oxidative stress and abrogated the subsequent alcohol-evoked increases in ROS and MDA levels in SO rats. Neither ethanol nor cyanamide influenced ROS or MDA levels in OVX rats. Importantly, cyanamide exaggerated ethanol-evoked hypotension in SO and uncovered this hypotensive response in OVX rats, which implicates ALDH2 in the vasodilating effect of ethanol.


CONCLUSIONS
Contrary to our hypothesis, cyanamide attenuated the E2 -dependent cardiac dysfunction caused by alcohol, likely by preconditioning the heart to oxidative stress, while exacerbating the vasodilating effect of alcohol. The latter might predispose to syncope when cyanamide and alcohol are combined in females.