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Biomedical subjects

R S Eliot

Publications and source records attributed to R S Eliot.

At least 19 recordsLinked to original sources
PubMed1992

Stress and the heart. Mechanisms, measurement, and management.

Unrelieved physical or mental stress and repeated episodic stress are ultimately harmful to the cardiovascular system and thus can be life-threatening. In this article, Dr Eliot describes efforts to quantify the psychophysiologic responses to stress and to identify the components of stress and its clinical consequences. He also explains the importance of controlling the real-life episodic fluctuations in blood pressure that occur daily in response to stress.

Animals↗
PubMed1979

Heterogeneity in distribution of cardiac glycogen following isoproterenol infusions in the dog.

A combined biochemical, histochemical and cytochemical study was made of cardiac glycogen distribution following intravenous infusions of varying doses of isoproterenol in anaesthetized, open-chested dogs. There was a dose-dependent decrease in glycogen levels in biopsies of the posterolateral wall of the left ventricle which also exhibited a transmural gradient with the endocardial third the most severely affected. Periodic acid-Schiff (PAS) histochemical studies also suggested a transmural gradient. There was, however, a marked variability within each layer, particularly the large amounts in the conduction system fibres. The ultrastructural studies exhibited a marked variation in glycogen content from one cell to the next. This was particularly evident in the complete absence of absence of granules in the contraction band lesions of isoproterenol cardiotoxicity yet substantial amounts were retained in neighbouring cells. Isoproterenol, therefore, produces a heterogenous depletion of cardiac glycogen related to the scattered catecholamine-induced myocardial cellular lesions. These relations have not previously been documented or emphasized.

Animals↗
PubMed1979

Temporal changes in endocardial energy metabolism following propranolol and the metabolic basis for protection against isoprenaline cardiotoxicity.

Propranolol infusions in open-chested, anesthetised dogs increased endocardial levels of ATP and phosphocreatine. It reduced ADP, AMP, glucose-6-phosphate and lactate in this region. Endocardial glycogen was transiently increased. Metabolic perturbations in the endocardium produced by cardiotoxic doses of isoprenaline were prevented or reduced by propranolol pretreatment. Thus, propranolol appears to have a more selective action on endocardial versus midmyocardial or epicardial metabolism.

Adenosine Diphosphate↗
PubMed1979

Transmural distribution of metabolites and blood flow in the canine left ventricle following isoproterenol infusions.

The effects of intravenous infusions of isoproterenol (0.1, 1.0 or 2.5 micrograms/kg/min for 1 hr) on the transmural distribution of myocardial high-energy phosphates and glycolytic intermediates were determined in anesthetized, open chested dogs. The transmural distribution of blood flow across the left ventricular wall was determined after serial injections of 15 mu radioactively labeled microspheres. A biopsy of the posterolateral wall was frozen in liquid nitrogen, divided into epicardial, midmyocardial and endocardial thirds, and assayed for metabolites. The remainder of the heart was processed for light and electron microscopy. At the infusion rate of 2.5 micrograms/kg/min, isoproterenol caused nonuniform reductions in ATP, phosphocreatine, total adenine nucleotides and glycogen, which were particularly depleted in the endocardium. Isoproterenol also caused nonuniform increases above baseline in blood flow (epicardial, 492%; midmyocardial, 197%; and endocardial, 131%). The endocardial/epicardial blood flow ratios, however, were reduced. Evidence of cellular damage was demonstrated by the presence of numerous contraction band lesions along with mitochondrial swelling and the appearance of electron-dense deposits. It is concluded that necrogenic infusions of isoproterenol impair myocardial energy production in all myocardial layers despite an overall increase in blood flow. There appears to be a link between the gradients in metabolites and the distribution of blood flow such that the endocardium becomes more vulnerable to injury.

Animals↗
PubMed1978

Sudden death and acute myocardial infarction: clues to differences in pathophysiology.

Although both sudden death and acute myocardial infarction are almost always associated with long-standing obstructive coronary artery disease, both may originate in the myocardium. Spasm has been suggested as a factor contributing to sudden death. Not all persons dying of acute myocardial infarction have narrowed coronary arteries, nor do all persons with obstructed arteries die of heart disease. The first phase of acute myocardial infarction may well involve myocardial necrosis, followed by stasis and collapse of collateral circulation and occasionally by coronary occlusion.

Acute Disease↗
PubMed1977

Stress and cardiovascular disease.

Currently the role of stress as a potential factor in cardiovascular disease is receiving considerable attention. Accordingly, it is important to know how it is defined and identified, how it affects the cardiovascular system and how it can be managed with the knowledge presently available. An overview of the present body of knowledge on the relationship between stress and cardiovascular disease is presented for the reader's consideration.

Adrenergic beta-Antagonists↗
PubMed1977

Influence of environmental stress on pathogenesis of sudden cardiac death.

The effects of 20th-century stress on the cardiovascular system are reviewed and correlated with experimental animal models. A classic example of such stress is drawn from a study of the aerospace workers at Cape Kennedy who were shown to be exposed to excessive occupational stress. Surprisingly, the usual risk factors did not predict a greater risk, yet the population exhibited a higher incidence of sudden cardiac death and acute myocardial infarction. Acute myocardial necrosis was much more frequently demonstrated than was acute coronary obstruction of any type. Retrospective coroner's studies revealed two types of myocardial necrosis: 1) elongated, thinned or wavy fibers and 2) anomalous contraction bands. Correlation of these clinical observations with experimental data was duplicated in canine models of myocardial infarcion and/or catecholamine-induced necrosis. Catecholamines can lead to irreversible myocardial necrosis but the underlying mechanisms appear to be complex. Extrapolation of the results from the experimental and clinical studies suggests that environmental stress can lead to myocardial necrosis.

Adenosine Triphosphate↗
PubMed1976

Reduced high-energy phosphate levels in rat hearts. I. Effects of alloxan diabetes.

Significant alterations in heart carbohydrate and lipid metabolism are present 48 h after intravenous injection of alloxan (60 mg/kg) in rats. It has been suggested that uncoupling of oxidative phosphorylation occurs in the alloxanized rat heart in vivo, whereas normal oxidative metabolism has been demonstrated in alloxan-diabetic rat hearts perfused in vitro under conditions of adequate oxygen delivery. We examined the hypothesis that high-energy phosphate metabolism might be adversely affected in the alloxan-diabetic rat heart in vivo. Phosphocreatine and ATP were reduced by 58 and 45%, respectively (P is less than 0.001). Also, oxygen-dissociation curves were shifted to the left by 4 mmHg, and the rate of oxygen release from blood was reduced by 21% (P is less than 0.01). Insulin administration normalized heart high-energy phosphate compounds. ATP production was accelerated in diabetic hearts perfused in vitro with a well-oxygenated buffer. These studies support the hypothesis that oxidative ATP production in the alloxan-diabetic rat heart is reduced and suggest that decreased oxygen delivery may have a regulatory role in the oxidative metabolism of the diabetic rat heart.

Adenosine Diphosphate↗