The nonvascular metabolic myocardial vulnerability factor in “coronary heart disease”

Raab, W.

doi:10.1016/0002-8703(63)90327-2

Cited by 72 publications

(25 citation statements)

References 142 publications

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“…The intriguing hypothesis proposed by Raab and colleagues that physical inactivity causes deterioration of vagal and sympathoinhibitory counterregulation against oxygen-wasting adrenergic preponderance warrants further investigation. 35 Serum lipids. The influence of increased physical activity on various serum lipids, especially serum cholesterol, has not been definitively established.…”

Section: How Physical Activity May Have An Influencementioning

confidence: 99%

Physical activity and the prevention of coronary heart disease

Fox

Naughton

1972

Preventive Medicine

295

313

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Section: How Physical Activity May Have An Influencementioning

confidence: 99%

Physical activity and the prevention of coronary heart disease

Fox

Naughton

1972

Preventive Medicine

295

313

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“…INTRODUCTION Increasing attention has been given to measures which might protect the heart during acute coronary occlusion and limit the size of the subsequent infarction. There is evidence to suggest that the ultimate extent of myocardial necrosis after acute coronary occlusion is determined by the balance between oxygen supply and demand in the areas of myocardium supplied by the vessel (1). Because myocardial ischemic injury is irreversible (2) long before the extent of collateral flow has increased significantly (3,4), a reduction in the oxygen requirement of the infarcted area until establishment of collateral flow would be an attempt to limit the extent of myocardial injury.…”

mentioning

confidence: 99%

Effect of Inhibition of Lipolysis on Infarct Size After Experimental Coronary Artery Occlusion

Kjekshus¹,

Mjøs²

1973

J. Clin. Invest.

115

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A B S T R A C T Recent studies have demonstrated a depressant effect of increased delivery of FFA to the hypoxic heart. Because catecholamines are released in acute myocardial infarction, it is likely that lipolytic activity is increased. The purpose of this study was to determine whether inhibition of hormone-sensitive lipases influence the extent and severity of myocardial ischemic injury produced by coronary occlusion. Myocardial infarction was produced by occlusion of the left anterior descending coronary artery in open-chest dogs. 15 min later a surface map of S-T segments was obtained with the use of 10-14 epicardial leads in the distribution area of the occluded artery. Average S-T segment elevation of all sites was used as an index of myocardial ischemic injury. Before coronary occlusion, the average S-T segment elevation was 0.340.2, which increased to 4.1+0.7 mV (SEM, 12 dogs) after occlusion. Inhibition of lipolytic activity by P-pyridyl-carbinol before repeated coronary occlusion reduced the occlusion-induced S-T segment elevation to 2.1+0.6 mV (P <0.001). When arterial concentrations of FFA were raised by i.v. infusion of a triglyceride emulsion and heparin, average S-T segment elevation after coronary occlusion increased from 1.2±0.7 to 2.2±0.8 mV (P < 0.05) in animals treated with P-pyridyl-carbinol, which suggests an unfavorable effect of circulating FFA in this setting. Isoproterenol given before a repeated occlusion increased the severity and extent of the ischemic injury. The effect of isoproterenol on the occlusion-induced S-T segment elevation was reduced, however, when the lipolytic effect of the drug was inhibited by P-pyridyl-carbinol.Our study suggests that P-pyridyl-carbinol during acute coronary artery occlusion may be of importance in reducing the extent and severity of myocardial ischemic injury.

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“…R aab [15,18] Sobel [16], R aab et al [17], H arris [19], van Vliet et al [20] have shown that the increased release of catecholamines combined with an adrenocortical excess does not only contribute to arterial atherogenesis but can also produce a myocardiotoxic action.…”

Section: Discussionmentioning

confidence: 99%

Corticoadrenal and Adrenergic Overactivity and Hyperlipidemia in Prolonged Emotional Stress

Argüelles¹,

Martínez²,

Hoffman³

et al. 1972

Horm Res Paediatr

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A group of 23 Air Force Lieutenant Colonels who attended a long General Staff Course were studied with assays of blood lipid fractions, 11-hydroxycorticoids and excretion of epinephrine, norepinephrine, free 11-hydroxycorticoids, 17-hydroxycorticoids (17-OHCS), dehydroepiandrosterone (DHA) and 17-ketosteroids (17-KS). More or less continuous emotional stress was expected as most of these subjects had familiar responsabilities and the course was extremely competitive, with a large percent of dropouts. This meant, for most of these officers, the end of their careers. Norepinephrine levels were significantly increased and correlated with aggressive behaviour. Significant (p < 0.001) elevations of plasma and urine-free 11-hydroxycorticoíds were registered showing levels in the range found in very stressed subjects. Blood total lipids and cholesterol raised significantly during the course, with levels comparable to those found in hyperlipidemic patients with coronary arteriopathy. The EKG changes were not significant. The possibility that this maintained stressful state might cause a hyperlipoproteinemia and consequent atheromatosis and coronariopathy is discussed.

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The nonvascular metabolic myocardial vulnerability factor in “coronary heart disease”

Cited by 72 publications

References 142 publications

Physical activity and the prevention of coronary heart disease

Physical activity and the prevention of coronary heart disease

Effect of Inhibition of Lipolysis on Infarct Size After Experimental Coronary Artery Occlusion

Corticoadrenal and Adrenergic Overactivity and Hyperlipidemia in Prolonged Emotional Stress

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