Combined acetaldehyde and nicotine exposure depresses cardiac contraction in ventricular myocytes: prevention by folic acid.

Journal Article (Journal Article)

Chronic alcoholism can progress to alcoholic cardiomyopathy characterized by ventricular dilation and impaired ventricular contractility. Nicotine abuse continues to remain a serious risk factor for cardiovascular diseases. However, little is know regarding the combined effects. This study was designed to examine the role of short-term combined exposure of the main alcohol metabolite acetaldehyde (ACA) and nicotine on cardiac contractile function in adult rat ventricular myocytes, and if folate exposure attenuates the effect of ACA/nicotine. Mechanical and intracellular Ca2+ properties were evaluated by an IonOptix SoftEdge system. Short-term (4-6 h) culture of myocytes with ACA (10 microM), nicotine (100 microM), or combination of the two in sealed vials with silicone septa depressed maximal velocity of shortening/relengthening, without affecting duration of shortening/relengthening and intracellular Ca2+ handling. Interestingly, the toxin-induced defects on myocyte mechanical properties were ablated with cotreatment of folate (100 microM), an essential vitamin required for DNA synthesis and repair. Collectively, these data provided evidence that ACA and nicotine, either alone or in combination, directly depressed cardiomyocyte mechanical function possibly through mechanisms related to DNA damage.

Full Text

Duke Authors

Cited Authors

  • Aberle, NS; Privratsky, JR; Burd, L; Ren, J

Published Date

  • November 2003

Published In

Volume / Issue

  • 25 / 6

Start / End Page

  • 731 - 736

PubMed ID

  • 14624973

International Standard Serial Number (ISSN)

  • 0892-0362

Digital Object Identifier (DOI)

  • 10.1016/


  • eng

Conference Location

  • United States