Myocardial uptake of free fatty acids and carbohydrates after beta adrenergic blockade

Marchetti, G; Merlo, L; Noseda, V.

doi:10.1016/0002-9149(68)90121-5

Cited by 32 publications

(3 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It has previously been shown that especially non-selective beta-blockers reduce plasma FFA levels by counteracting the beta-adrenoceptor mediated lipolysis (18,5,6,27,35) and also reduce myocardial FFA uptake (9,14,22). Accordingly, the purpose of this study was to evaluate the influence of different beta-blockers on the myocardial FFA uptake in the normal and occluded dog heart by using radioaetively labeled iodoheptadecanoic acid ( 1 3 1 I-HDA), a stearic acid analogue with similar metabolic behaviour as the normal compound (26,13).…”

Section: Zusammenfassungmentioning

confidence: 99%

Metabolic Consequences of Beta-Adrenergic Receptor Blockade for the Acutely Ischemic Dog Myocardium

Westera¹,

Wall²,

Eenige³

et al. 1984

Nuklearmedizin

View full text Add to dashboard Cite

SummaryIn an experimental study in 50 dogs the myocardial uptake of free fatty acids (FFAs) after beta-blockade was determined using radioiodinated heptadecanoic acid as a metabolic tracer. All 4 beta-blockers used (metoprolol, timolol, propranolol and pindolol) lowered the uptake of FFAs in the normal canine heart. Uptake of FFAs was also diminished after coronary artery occlusion per se, but administration of beta-blockers exerted little additional influence on the uptake of FFAs. This observation was qualitatively parallelled by the uptake of 201T1 in concomitant experiments. Plasma FFA levels were increased by pindolol (non-selective with intrinsic sympathomimetic activity), not changed by metoprolol (a cardioselective betablocking agent) and lowered by timolol and propranolol (both nonselective compounds). The extent of ischemic tissue, as reflected by uptake of iodoheptadecanoic acid and 201T1, was diminished by metoprolol but not by other beta-blockers. Regional distribution of both tracers, as shown in the endo-epicardial uptake ratios, was hardly influenced by beta-blockade, except for a small increase of 201T1 uptake in non-occluded endocardium. Uptake of 201T1 as well as of iodoheptadecanoic acid in the ischemic area was increased by metoprolol, timolol and propranolol and decreased by pindolol. We conclude that beta-blocking agents confer different effects on myocardial uptake and metabolism of FFAs which might possibly be related to their different inherent properties.

show abstract

Section: Zusammenfassungmentioning

confidence: 99%

Metabolic Consequences of Beta-Adrenergic Receptor Blockade for the Acutely Ischemic Dog Myocardium

Westera¹,

Wall²,

Eenige³

et al. 1984

Nuklearmedizin

View full text Add to dashboard Cite

show abstract

“…Although the regulation of the metabolism of the ischaemic myocardium is a controversial issue (Hjalmarsson & Werko, 1975;Wildenthal et al, 1976) there are indications that myocardial ischaemic injury can be reduced by measures favouring carbohydrate metabolism (Oliver et al, 1968;Mjos, 1976). Propranolol has been found to reduce myocardial uptake of free fatty acids with a consequent relative rise in the myocardial carbohydrate utilization (Marchetti et al, 1968;Masters & Glaviano, 1969). This should be expected to raise the cardiac respiratory quotient (McKenna et al, 1966), indicating an oxygen-saving shift of myocardial energy metabolism.…”

Section: Effects In Patients With Angina Pectorismentioning

confidence: 99%

Mode of Action of Beta Blockers in Angina Pectoris

Åblad¹,

Carlsson²,

Ek³

et al. 1977

Scott Med J

View full text Add to dashboard Cite

The therapeutic effect of beta adrenoceptor blockers in angina pectoris can be ascribed to an inhibition of beta1 receptor mediated stimulation of heart rate and myocardial contractility, resulting in an improved oxygen supply-demand balance in the myocardium. When given in equipotent beta1 blocking doses, the nonselective blocker propranolol and the beta1 selective blocker metoprolol differ markedly as regards inhibition of adrenaline induced beta2 mediated vasodilatation. Only propranolol will inhibit this effect. After propranolol, adrenaline therefore elicits a haemodynamic effect pattern characterized by high peripheral vascular resistance, high arterial blood pressure, low cardiac output and increased cardiac size. In view of these findings it is suggested that a beta1 selective blocker may be a more efficient antianginal agent than a nonselective blocker in those patients in which the anginal attack is associated with a significant release of adrenaline. The clinical relevance of this hypothesis has not been tested.

show abstract

“…It is reasonable, however, to postulate that rebound /3-adrenergic hypersensitivity is most likely to be unmasked during acute myocardial infarction, a condition characterized by marked elevation of both plasma25-27 and local myocardial catecholamine levels. 28,29 In this situation too, urgent questions regarding the relative risks of abrupt withdrawal vs continuation of /3-blockers frequently arise. This report describes the hospital course and prospectively collected measurements of infarct size, left ventricular function, and cardiac arrhythmias in clinically comparable groups of patients with acute myocardial infarction with and without abrupt withdrawal of /3-blockade.…”

mentioning

confidence: 99%

Abrupt withdrawal of beta-blockade therapy in patients with myocardial infarction: effects on infarct size, left ventricular function, and hospital course.

et al. 1986

View full text Add to dashboard Cite

The effects of abrupt withdrawal or continuation of fl-blockade therapy during acute myocardial infarction were evaluated in 326 patients participating in the Multicenter Investigation of the Limitation of Infarct Size (MILIS). Thirty-nine patients previously receiving a f8-blocker and randomly selected for withdrawal of fl-blockers and placebo treatment during infarction (group 1) were compared with 272 patients previously untreated with fl-blockers who were also randomly assigned to placebo therapy (group 2). There were no significant differences between the two groups in MB creatine kinase isoenzyme (15.8 10.9 vs 18.2 + 14.4 g-eq/m2, respectively) estimates of infarct size, radionuclide-determined left ventricular ejection fractions within 18 hr of infarction (0.44 0.15 vs 0.47 0.16) or 10 days later (0.42 0.14 vs 0.47 0.16), creatine kinase-determined incidence of infarct extension (13% vs 6%), congestive heart failure (43% vs 37%), nonfatal ventricular fibrillation (5% vs 7%), or in-hospital mortality (13% vs 9%). Patients in group 1 had more recurrent ischemic chest pain (p = .002) within the first 24 hr after infarction, but not thereafter. However, this did not appear to be related to a rebound increase in systolic blood pressure, heart rate, or double product. In a separate analysis, 20 propranolol-eligible group 1 patients randomly selected for withdrawal of fl-blockade (group 3) were compared with 15 patients randomly selected for continuation of prior fiblockade therapy (group 4). This comparison yielded similar results. These data indicate that the ,f-blockade withdrawal phenomenon is not a major clinical problem in patients with acute myocardial infarction. f-Blockade therapy can be discontinued abruptly during acute myocardial infarction if clinically indicated.

show abstract

Myocardial uptake of free fatty acids and carbohydrates after beta adrenergic blockade

Cited by 32 publications

References 22 publications

Metabolic Consequences of Beta-Adrenergic Receptor Blockade for the Acutely Ischemic Dog Myocardium

Metabolic Consequences of Beta-Adrenergic Receptor Blockade for the Acutely Ischemic Dog Myocardium

Mode of Action of Beta Blockers in Angina Pectoris

Abrupt withdrawal of beta-blockade therapy in patients with myocardial infarction: effects on infarct size, left ventricular function, and hospital course.

Contact Info

Product

Resources

About