The acute metabolic and hemodynamic responses of the left ventricle to ethanol.

Regan, Richard J.; Koroxenidis, Gabriel T.; Moschos, Christos B.; Oldewurtel, Henry A.; Lehan, Patrick H.; Hellems, Harper K.

doi:10.1172/jci105340

Cited by 212 publications

(41 citation statements)

References 32 publications

(37 reference statements)

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“…Ethanol exerts a negative inotropic action in isolated perfused hearts (45), but its hemodynamic effects in intact animals are controversial. Myocardial function and coronary blood flow have been said to increase (46,47) and to decrease (48,49) after ethanol administration. It has been postulated that the positive inotropic effect of ethanol in vivo is caused by the sympathomimetic action of acetaldehyde (50), the immediate product of ethanol oxidation.…”

Section: Resultsmentioning

confidence: 99%

Metabolic Control of the Circulation

Liang¹,

Lowenstein²

1978

J. Clin. Invest.

123

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A B S T R A C T Chloralose-anesthetized dogs were infused intravenously with either Tris-acetate or Trispyruvate at 0.0375, 0.075, and 0.15 mmol/kg per min successively, each for 20 min. Acetate infusion increased cardiac output, left ventricular dP/dt and dPldt/P, and coronary blood flow, while pyruvate infusion did not. Infusions of either substance increased arterial blood and skeletal muscle concentrations of citrate and malate, but only acetate infusion increased the tissue AMP content and decreased the ATP:AMP ratio. The increase in cardiac output produced by acetate was accompanied by an increase in total body oxygen consumption and a decrease in the difference between arterial and mixed venous blood oxygen.Myocardial oxygen consumption increased during acetate infusion, but the decrease in myocardial oxygen extraction and the increase in coronary sinus blood oxygen saturation suggest that an active coronary vasodilation which was not a result of the increased cardiac work, occurred. The concentration of hypoxanthine in the coronary sinus and the content of myocardial adenosine increased, which suggests that the increase in coronary blood flow was caused by the vasodilator action ofadenosine released from the myocardium, and that adenosine production is not necessarily tied to Po2.These systemic and coronary hemodynamic changes also occurred when acetate (0.075 mmol/kg per min) was infused into conscious dogs. Acetate infusion also increased blood flow to the gastrointestinal tract, kidneys, intercostal muscle, and diaphragm. These changes were not affected by propranolol pretreatment, but were abolished by pretreatment with fluoroacetate which reduced acetate oxidation.These results suggest that the circulatory stimulation produced by acetate was not caused by increases in

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Section: Resultsmentioning

confidence: 99%

Metabolic Control of the Circulation

Liang¹,

Lowenstein²

1978

J. Clin. Invest.

123

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“…The requirements for valid interpretation of arteriovenous differences were met after the 1st hr of alcohol (19,20) LEFT VENTRICULAR END-DIASTOLIC PRESSURE (mmHg) FIGuRE 2 Left ventricular response to angiotensin in alcoholics without heart failure. The alcoholic subject without clinical evidence of cardiac disease exhibited a nearly threefold rise of ventricular end-diastolic pressure but only a minimal stroke output and stroke work increment.…”

Section: Methodsmentioning

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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“…Ethanol may diminish myocardial function (13). Furthermore, an excessive mortality has been noted in patients with pneumonia when alcoholism was present (14).…”

Section: Resultsmentioning

confidence: 99%