Premium
Oxidative stress level mediates the inotropic effects of alcohol on the heart
Author(s) -
AlRubaiee Mustafa,
Umoh Nsini,
Jeffress Miara,
Walker Robin,
Cousins Valerie,
Haddad Georges E
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1126.10
Subject(s) - oxidative stress , inotrope , medicine , alcoholic cardiomyopathy , alcohol , cardiac function curve , cardiology , oxidative phosphorylation , ventricle , cardiomyopathy , endocrinology , dilated cardiomyopathy , binge drinking , anesthesia , heart failure , chemistry , alcohol consumption , biochemistry
Alcohol has deleterious as well as beneficial cardiac effects depending on the exposure level, length and frequency. Binge drinking can be associated with significant cardiac dysfunction depending on the amount of alcohol consumption. Thus, the objective of this study is to evaluate the role of acute alcohol‐induced oxidative stress in altering cardiac function in vivo. Anesthetized adult rats were infused with (% w/v) low (LA: 0.023%), moderate (MA: 0.115%) or high (HA: 0.461%) alcohol levels through the jugular vein while measuring the pressure‐‐volume loop with a conductance catheter apically inserted in the left ventricle. Isolated cardiocytes were used for oxidative stress assays. LA increases ESPVR at a maintained EDV and SV and reduced oxidative stress, whereas MA and HA did not affect ESPVR but increased EDV, SV and oxidative stress. Furthermore, LA reduced stroke work and PVA whereas MA and HA increased these energy parameters. Interestingly, MA and HA increased cardiac compliance. We conclude that acute MA or HA increases cardiac compliance with oxidative stress at an elevated energy cost, whereas LA has the opposite effect. This seemingly compensatory compliance response could be outweighed by cardiac overwork in chronic alcohol leading to dilated alcoholic cardiomyopathy. This work was supported in part by grants NIH/NIAAA/1R15AAA019816–01A1 and 2G12 RR003048 RCMI/NCRR/NIH.