Hemodynamic and metabolic effects of chronic alcoholism in man

Wendt, Vernon E.; Wu, Clyde; Balcon, Raphael; Doty, Gordon; Bing, Richard J.

doi:10.1016/0002-9149(65)90452-2

Cited by 97 publications

(14 citation statements)

References 30 publications

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“…Our data, based on analysis of heart muscle, confirm the results of Wendt et al [1965], who studied metabolic changes in the blood of chronic alcoholic men. Estimating the enzyme activity in arterial and coronary sinus blood, they found that chronic ingestion of ethanol pro voked damage to the myocardial cell membrane.…”

Section: Discussionsupporting

confidence: 88%

Effect of Ethanol on the Metabolism of the Myocardium and its Relationship to Development of Alcoholic Myocardiopathy

A¹,

Bada²,

Krutý³

et al. 1973

Cardiology

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The effect of ethanol on the metabolism of the heart muscle was studied in two series of experiments in the rat. In an acute model, a single injection of 250 mg ethanol/l00 g body weight was given intraperitoneally. Blood glucose, lactate, NEFA, and myocardial glycogen content were analyzed at 15, 30, and 60 min. All these parameters increased when measured 15 and 30 min after the ethanol injection, but they all returned to normal levels at 60 min. A model of chronic alcohol intake was investigated for 10 weeks. The same dose of ethanol was injected daily to the experimental animals whereas the control rats received an isocaloric dose of glucose. Chronic administration of ethanol caused changes not only in the glycolytic cycle of the myocardium (diminished glycolytic activity), but also in the oxidative phosphorylation of myocardial mitochondria (decrease of homogenate and mitochondria respiration as well as of respiratory control ratio of isolated mitchondria).

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Section: Discussionsupporting

confidence: 88%

Effect of Ethanol on the Metabolism of the Myocardium and its Relationship to Development of Alcoholic Myocardiopathy

A¹,

Bada²,

Krutý³

et al. 1973

Cardiology

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“…Since lipid accumulation in heart muscle is one of the consequences of acute alcohol ingestion during the production of transient myocardial injury in the experimental animal (20), a possible role of triglyceride accumulation through an alteration of membrane or myofibrillar function may be considered (29). The decline in myocardial extraction of free fatty acid repeatedly observed (20,23,30) and the associated increased extraction of plasma triglyceride suggests that altered lipid transport may be an important determinant of this process.…”

Section: Restyltsmentioning

confidence: 99%

Ventricular function in noncardiacs with alcoholic fatty liver: role of ethanol in the production of cardiomyopathy

Regan¹,

Levinson²,

Oldewurtel³

et al. 1969

J. Clin. Invest.

225

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A B S T R A C T Since many patients with cardiomyopathy have a history of chronic ethanolism often associated with malnutrition, we have evaluated left ventricular (LV) function in alcoholics with fatty liver, who had no clinical evidence of cardiac or nutritional disease.During an afterload test of LV function the pressor response to angiotensin evoked a threefold rise of enddiastolic pressure in the alcoholic group which was substantially greater than the 4 mm Hg rise in control subjects. The stroke volume and stroke work response in the noncardiac alcoholic was significantly less than in controls. Diminished LV function was corroborated in the noncardiac alcoholic at rest, using a contractility index.To evaluate the dose-response relationship of ethanol in the production of cardiac malfunction, two groups of noncardiac alcoholic subjects were studied acutely at low and moderate dose levels. After 6 oz, ventricular function, myocardial blood flow, and metabolism were not significantly affected. After 12 oz, there was a progressive rise of end-diastolic pressure and decrease of stroke output at a mean blood alcohol level of 150 mg/ 100 ml, reverting toward control by 4 hr. The coronary effluent transiently evidenced leakage of cell constituents, despite an increase of coronary blood flow, suggesting a direct but reversible cardiac injury. Myocardial extraction of triglyceride was enhanced, whereas FFA uptake was reduced. A possible role of myocardial triglyceride accumulation in heart muscle was considered in pathogenesis.Chronic ingestion of 16 oz of Scotch daily by an alcoholic subject while on a normal diet-produced, after 12 wk, a progressive increase of heart rate and size,

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“…The chronic effect of alcohol on the heart has been the subject of a series of investigations (1)(2)(3)(4). In general, the conclusion was reached that alcohol has a direct toxic effect on the heart muscle.…”

Section: Introductionmentioning

confidence: 99%

“…Received for publication 26 February 1973 and in revised form 18 June 1973. changes (3,(5)(6)(7)(8). It has been shown, for example, that in the heart of alcoholic patients, as well as in that of animals exposed to large doses of alcohol, electronmicroscopic observations of mitochondria reveal defects which resulted in enzymatic changes within these structures, affecting the whole intracellular metabolic state.…”

Section: Introductionmentioning

confidence: 99%

The Effect of Prolonged Administration of Ethanol on Cardiac Metabolism and Performance in the Dog

Pachinger¹,

Tillmanns²,

Mao³

et al. 1973

J. Clin. Invest.

Self Cite

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A B S T R A C T The effect of prolonged administration of alcohol on mitochondrial function and high-energy phosphate (ATP) of heart muscle was investigated in dogs. Animals were divided into two groups, a control group and a group that received alcohol. In the experimental series, dogs received 400 ml of a 25% solution of alcohol added to the food and drinking water. Measurements were carried out after ethanol had been withheld for 2 days. Total myocardial blood flow, cardiac output, and myocardial 02 consumption remained at control levels. Measurement of cardiac contractility using the maximal rate of left ventricular pressure rise (dP/dtmax) showed no change in animals exposed to alcohol. When the afterload of the heart was increased with angiotensin, a slight but not significant decline in cardiac contractility was observed. Activities of various intramitochondrial and extramitochondrial enzymes were measured in both groups. After alcohol administration, the primarily intramitochondrial isocitrate dehydrogenase diminished. ATP in heart muscle of dogs exposed to alcohol declined, and mitochondrial oxygen consumption and respiratory control indices diminished. These observations suggest that the primary lesion leading to alteration of myocardial performance is a biochemical malfunction of the mitochondria, which at this early stage is not reflected in changes in myocardial contractility.

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Hemodynamic and metabolic effects of chronic alcoholism in man

Cited by 97 publications

References 30 publications

Effect of Ethanol on the Metabolism of the Myocardium and its Relationship to Development of Alcoholic Myocardiopathy

Effect of Ethanol on the Metabolism of the Myocardium and its Relationship to Development of Alcoholic Myocardiopathy

Ventricular function in noncardiacs with alcoholic fatty liver: role of ethanol in the production of cardiomyopathy

The Effect of Prolonged Administration of Ethanol on Cardiac Metabolism and Performance in the Dog

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