Alcohol and Alcoholism Vol. 37, No. 1, pp. 30-37, 2002
© 2002 Medical Council on Alcohol
INFLUENCE OF PRENATAL ALCOHOL EXPOSURE ON MYOCARDIAL CONTRACTILE FUNCTION IN ADULT RAT HEARTS: ROLE OF INTRACELLULAR CALCIUM AND APOPTOSIS
Department of Pharmacology, Physiology, and Therapeutics, University of North Dakota School of Medicine, Grand Forks, ND 58203,
1 Departments of Physiology,
2 Obstetrics & Gynecology, Wayne State University School of Medicine, Detroit, MI 48201 and
3 Department of Biology, Morgan State University, Baltimore, MD 21251, USA
Received 23 April 2001; first review notified 6 July 2001; accepted 8 August 2001
— To assess the teratogenic action of ethanol on cardiac contractile function in offspring exposed to ethanol in utero, pregnant Sprague–Dawley rats were fed with ethanol during gestation. Left-ventricular papillary muscles and myocytes were isolated from the offspring of the ethanol-ingesting and control pregnant rats. Mechanical parameters measured were peak tension development (PTD, indicating the myocardial force-generating capacity), peak cell shortening (PS), time-to-PTD/PS (TPT/TPS), time-to-90% relaxation/re-lengthening (RT90/TR90), and maximal velocities of contraction/shortening and relaxation/re-lengthening (±VT and ±dL/dt). Intracellular Ca2+ levels and apoptosis were evaluated with fura-2 fluorescent dye and Caspase-3 activation assay, respectively. Offspring of the ethanol group displayed decreased heart weight associated with comparable body, liver and kidney weight, and papillary muscle weight/size, compared to the control group. However, prenatal ethanol exposure depressed myocardial PTD and ±VT. The myocardium from the ethanol group also exhibited slightly but significantly shortened TPT, accompanied with normal RT90. Muscles from both groups exhibited comparable responses to post-rest potentiation, increasing extracellular Ca2+ concentration, noradrenaline and acute ethanol challenge. Ventricular myocytes from both the control and ethanol groups possessed similar PS, TPS, TR90 and ±dL/dt. Both resting and peak intracellular Ca2+ levels were elevated in myocytes from the ethanol group. Additionally, acute ethanol application depressed caffeine-induced intracellular Ca2+ rise in myocytes from both groups. Myocytes from the ethanol group displayed an enhanced Caspase-3 activation, compared to control myocytes. These results suggest that prenatal ethanol exposure alters myocardial contractile function and may contribute to the development of postnatal cardiac dysfunction through, in part, increased intracellular Ca2+ loading and apoptosis.
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