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Cardiac contractile and sarcoplasmic reticulum function after acute ethanol consumption
1Department of Surgery, University of Texas Southwestern Medical Center, Dallas, 75235-9031, USA.
The Journal of Surgical Research
|August 1, 1996
Summary
Acute ethanol exposure depresses cardiac function by impairing sarcoplasmic reticulum calcium uptake, not calcium ATPase activity. This suggests ethanol uncouples ATP hydrolysis from calcium transport in the heart.
Area of Science:
- Cardiology
- Biochemistry
- Pharmacology
Background:
- Myocardial contractility relies on sarcoplasmic reticulum (SR) calcium regulation.
- Acute ethanol exposure is known to cause myocardial depression.
- The precise mechanism of ethanol's cardiac effects requires further investigation.
Purpose of the Study:
- To investigate if acute ethanol alters sarcoplasmic reticulum (SR) calcium pump function.
- To determine the impact of ethanol on myocardial contractility and SR calcium handling.
- To elucidate the mechanism behind ethanol-induced myocardial depression.
Main Methods:
- Adult guinea pigs were administered ethanol intravenously.
- Left ventricular (LV) function was assessed using the Langendorff preparation.
- SR calcium ATPase activity and calcium uptake were measured in isolated SR vesicles.
Main Results:
- Ethanol significantly reduced peak systolic left ventricular pressure (LVP) and maximal positive and negative dP/dt.
- Ethanol-treated hearts showed reduced contractile function even at maximal isoproterenol stimulation.
- SR calcium uptake was decreased by 25% in ethanol-treated hearts, while SR calcium ATPase activity remained unchanged.
Conclusions:
- Acute ethanol administration depresses cardiac contractile function.
- Ethanol impairs SR calcium uptake without affecting SR calcium ATPase activity.
- Ethanol likely uncouples ATP hydrolysis from calcium transport in the SR, contributing to myocardial depression.