Effect of ethanol and acetaldehyde on the (Na+ + K+)-activated adenosine triphosphatase activity of cardiac plasma membranes

Williams, Joseph W.; Tada, Michihiko; Katz, Arnold M.; Rubin, Emanuel

doi:10.1016/0006-2952(75)90308-1

Cited by 74 publications

(6 citation statements)

References 20 publications

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“…Ethanol has been shown to inhibit the Na+,K+-dependent ATPase of cardiac cell membranes [28]; however, the lack of change of the maximum diastolic potential in our study suggests that its inhibition may not contribute to changes in action potential pa rameters to any appreciable extent. In addi tion, such an inhibitory effect on the Na+, K+ ATPase would have been expected to in crease force development, however, we ob served a decrease in this study.…”

Section: Discussioncontrasting

confidence: 79%

A Moderate Concentration of Ethanol Alters Cellular Membrane Potentials and Decreases Contractile Force of Human Fetal Heart

Richards

Kulkarni²,

Brooks³

et al. 1989

Dev Pharmacol Ther

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The effects of ethanol, although well studied in the adult myocardium, have been little studied in fetal tissue. Experiments in pregnant animals suggest that ethanol compromises fetal myocardial performance, in utero; however, the physiological mechanism(s) remains obscure. The present report examines, in vitro, the effects of a moderate concentration of ethanol (20 mM) directly on cell membrane potentials and contractility of human fetal left ventricle as determined using intracellular microelectrodes and microforce transducers. We observed significant decreases in action potential amplitude, upstroke velocity, duration of repolarization, and the force of contractions. These effects were reversible. As ethanol crosses the placenta, our findings suggest that moderate concentrations of ethanol, as occur during 'social drinking', may temporarily compromise fetal myocardial performance in utero.

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Section: Discussioncontrasting

confidence: 79%

A Moderate Concentration of Ethanol Alters Cellular Membrane Potentials and Decreases Contractile Force of Human Fetal Heart

Richards

Kulkarni²,

Brooks³

et al. 1989

Dev Pharmacol Ther

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“…Our data in cardiac muscle do not specify at what point in the troponin actomysin reaction alcohol acts. Ethanol has also been demonstrated to interfere with Na+/K+ pump activity and with sarcolemmal permeability, both perturbations leading to an increase in [Na+]i (26)(27)(28)(29). It is difficult to ascribe a negative inotropic effect of ethanol at the sarcolemma since the resultant increase in [Na+]i should lead to an increase in [Ca2+]i through Na+/Ca2+ exchange.…”

Section: Discussionmentioning

confidence: 99%

Mechanism of myocardial contractile depression by clinical concentrations of ethanol. A study in ferret papillary muscles.

Guarnieri¹,

Lakatta²

1990

J. Clin. Invest.

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Moderate alcohol intoxication in man, a ubiqitious social event, causes acute but reversible myocardial depression, the mechanism of which is unknown. We investigated whether this depression could be due to a direct effect of ethanol on the process of electromechanical coupling by simultaneously measuring the transmembrane action potential and contraction, or the cytosolic calcium transient (via aequorin photoluminescence) and contraction in isolated ferret right ventricular papillary muscle. Ethanol, in concentrations that are similar to plasma levels in man during intoxication (0.15 vol %), de-pressed the force of contraction -10%. The step in the electromechanical process that was affected appeared to be the calcium-myofilament interaction, as there was no change in the transmembrane action potential or cytosolic calcium transient. This inhibition was quickly reversed by removal of the ethanol from the perfusate.On the other hand, higher concentrations of ethanol produced changes in contraction, the calcium transient, and the action potential, suggesting multiple levels of inhibition of electromechanical coupling. Increasing the perfusate calcium or use of the calcium channel agonist, BAY-K 8644, increased cytosolic calcium to near maximum but had little effect on contractility, confirming that the relationship between calcium and the myofilaments had been altered.These data suggest that the acute depression in ventricular function seen with alcohol consumption may be due to a direct effect on electromechanical coupling through inhibition of the calcium myofilament interaction. (J. Clin. Invest. 1990.

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“…Signs of muscle cell membrane abnormalities have frequently been observed in connection with exposure to ethanol both in chronic alcoholics and healthy individuals (2, [18][19][20]. The acute effect of ethanol on cell membranes is thought to be exerted by interaction with their lipid and protein compounds altering the membrane both structurally and functionally (21-24).…”

Section: Discussionmentioning

confidence: 99%

Ethanol Reduces Myoglobin Release during Isokinetic Muscle Exercise

Lundin

Hällgren

Lidell

et al. 1986

Journal of Internal Medicine

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Ethanol reduces myoglobin release during isokinetic muscle exercise. Acta Med Scand 1986; Changes in serum myoglobin concentrations were studied in 12 healthy males performing a standardized isokinetic 2-min exercise test. The test was performed on three separate occasions: in the habitual state, during moderate ethanol intoxication and one day after ethanol intake. Although the performed muscle work, maximal heart rate, and blood lactate levels did not differ between the three test occasions, the serum myoglobin increments after exercise were significantly reduced @<0.05) in the ethanol-intoxicated state and also 10-15 hours after ethanol intake. The reduction of the exercise-induced myoglobin increment was not explained by increased elimination of the protein. The mechanism, therefore, is likely to be a reduction of myoglobin release from skeletal muscle due to an ethanol-induced alteration of the muscle cell membrane, possibly by means of adenylate cyclase activation. Key words: ethanol, myoglobin, exercise.219: 415-9.

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Effect of ethanol and acetaldehyde on the (Na+ + K+)-activated adenosine triphosphatase activity of cardiac plasma membranes

Cited by 74 publications

References 20 publications

A Moderate Concentration of Ethanol Alters Cellular Membrane Potentials and Decreases Contractile Force of Human Fetal Heart

A Moderate Concentration of Ethanol Alters Cellular Membrane Potentials and Decreases Contractile Force of Human Fetal Heart

Mechanism of myocardial contractile depression by clinical concentrations of ethanol. A study in ferret papillary muscles.

Ethanol Reduces Myoglobin Release during Isokinetic Muscle Exercise

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