Effect of acute alcoholic intoxication on myocardial electrolyte and water distributions

Kischuk, Robert; Otten, Maureen; Polimeni, Philip I.

doi:10.1016/s0022-2828(86)80472-2

Cited by 12 publications

(2 citation statements)

References 31 publications

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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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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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“…Membranes from alcohol exposed muscle have impaired calcium uptake and release (Ohnishi et al ., 1985; Nicolas et al ., 1998; Cofan et al ., 2000). Additional indices of membrane function such as defective Na 2+ ‐K + ‐ATPase activities also occur (Ferguson et al ., 1984; Kischuk et al ., 1986; Lundin et al ., 1986). The targeting of membrane proteins by alcohol, such as voltage‐sensitive ion channel proteins, has been proposed (Oz and Frank, 1995).…”

Section: Animal Modelsmentioning

confidence: 99%

Alcoholic skeletal muscle myopathy: definitions, features, contribution of neuropathy, impact and diagnosis

Preedy

Adachi

Ueno

et al. 2001

Euro J of Neurology

148

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Alcohol misusers frequently have difficulties in gait, and various muscle symptoms such as cramps, local pain and reduced muscle mass. These symptoms are common in alcoholic patients and have previously been ascribed as neuropathological in origin. However, biochemical lesions and/or the presence of a defined myopathy occur in alcoholics as a direct consequence of alcohol misuse. The myopathy occurs independently of peripheral neuropathy, malnutrition and overt liver disease. Chronic alcoholic myopathy is characterized by selective atrophy of Type II fibres and the entire muscle mass may be reduced by up to 30%. This myopathy is arguably the most prevalent skeletal muscle disorder in the Western Hemisphere and occurs in approximately 50% of alcohol misusers. Alcohol and acetaldehyde are potent inhibitors of muscle protein synthesis, and both contractile and non-contractile proteins are affected by acute and chronic alcohol dosage. Muscle RNA is also reduced by mechanisms involving increased RNase activities. In general, muscle protease activities are either reduced or unaltered, although markers of muscle membrane damage are increased which may be related to injury by reactive oxygen species. This supposition is supported by the observation that in the UK, alpha-tocopherol status is poor in myopathic alcoholics. Reduced alpha-tocopherol may pre-dispose the muscle to metabolic injury. However, experimental alpha-tocopherol supplementation is ineffective in preventing ethanol-induced lesions in muscle as defined by reduced rates of protein synthesis and in Spanish alcoholics with myopathy, there is no evidence of impaired alpha-tocopherol status. In conclusion, by a complex series of mechanisms, alcohol adversely affects skeletal muscle. In addition to the mechanical changes to muscle, there are important metabolic consequences, by virtue of the fact that skeletal muscle is 40% of body mass and an important contributor to whole-body protein turnover.

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³¹P and ¹H magnetic resonance spectroscopy of acute alcohol cardiac depression in rats

Auffermann

Camacho

et al. 1988

Magnetic Resonance in Med

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Cardiac depression in the isolated rat heart perfused with 4% ethanol was correlated with intracellular phosphate energetics and tissue water distributions. Energy metabolites were assessed using 31P magnetic resonance spectroscopy (MRS) and correlated to the mitochondrial redox state using epicardial surface fluorometry. Changes in myocardial water compartmentation were measured by using 1H NMR spectroscopy with an extracellular chemical-shift reagent (DyTTHA) and correlated to results of 2D echocardiography (2DE). During alcohol perfusion there was a significant decrease in developed pressure and in coronary flow. No change was seen in ATP, PCr, pHi, Pi, or NADH. After withdrawal of alcohol from the perfusate cardiac function reverted to control values without a depletion of energy levels. During alcohol perfusion 1H MRS showed a marked redistribution of water from the intra- to the extracellular space, corresponding to a 35% left ventricular wall thinning confirmed by 2DE. The results indicate that acute alcohol cardiac depression is related to a dehydration of myocardial cells, but is not associated with intracellular acidosis or energy depletion.

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Effect of acute alcoholic intoxication on myocardial electrolyte and water distributions

Cited by 12 publications

References 31 publications

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

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

Alcoholic skeletal muscle myopathy: definitions, features, contribution of neuropathy, impact and diagnosis

³¹P and ¹H magnetic resonance spectroscopy of acute alcohol cardiac depression in rats

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Effect of acute alcoholic intoxication on myocardial electrolyte and water distributions

Cited by 12 publications

References 31 publications

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

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

Alcoholic skeletal muscle myopathy: definitions, features, contribution of neuropathy, impact and diagnosis

31P and 1H magnetic resonance spectroscopy of acute alcohol cardiac depression in rats

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³¹P and ¹H magnetic resonance spectroscopy of acute alcohol cardiac depression in rats