Key result
Acute ethanol exposure induced profound cardiac depression in isolated perfused rat hearts, and pregnancy neither exacerbated nor attenuated this cardiac toxicity.
Why the study?
Does pregnancy affect the cardiac toxicity of acute ethanol exposure in isolated perfused rat hearts?
Does pregnancy affect the cardiac toxicity of acute ethanol exposure in isolated perfused rat hearts?
In an isolated perfused rat heart model, pregnancy does not alter the profound cardiac depressive effects of acute ethanol exposure.
No pregnancy-specific modification of ethanol cardiotoxicity in this model; leaves open translation to human pregnancy and in vivo settings.
Numerous pregnant women are exposed to ethanol. Given the marked cardiovascular changes induced by pregnancy and the known cardiac toxicity of ethanol, we conducted this study to explore the effects of pregnancy on the cardiac toxicity of ethanol. Isolated, perfused rat hearts obtained from pregnant and nonpregnant Sprague-Dawley rats were exposed to increasing doses of ethanol (0.1, 0.2, 0.4, 0.6%). Heart rate, changes in left ventricular pressure over time (dP/dt), left ventricular systolic pressure, and coronary artery flow rate were measured. Ethanol induced profound cardiac depression in all parameters. Pregnancy neither exacerbated nor attenuated this cardiac toxicity. In the isolated perfused rat heart model, pregnancy does not affect the cardiac toxicity of acute ethanol exposure.
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Broughton et al. (1996) studied Pregnancy and acute ethanol exposure. Ethanol vs. Nonpregnant rat hearts was evaluated on Heart rate, changes in left ventricular pressure over time (dP/dt), left ventricular systolic pressure, and coronary artery flow rate. Acute ethanol exposure induced profound cardiac depression in isolated perfused rat hearts, and pregnancy neither exacerbated nor attenuated this cardiac toxicity.
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