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Biomedical subjects

M F Oliver

Publications and source records attributed to M F Oliver.

At least 145 records · Page 8Linked to original sources
PubMed1981

Metabolic aspects of rhythm disturbances.

[Profound alterations in metabolism occur within the first few minutes of myocardial ischaemia which may induce or modulate myocardial electrophysiological abnormalities and arrhythmogenesis, Fatty acid oxidation is inhibited with accumulation of long-chain acyl CoA esters and glycolysis is stimulated but later inhibited. This may be worsened by a peripheral sympathetic response. In particular regional variations in glycolytic ATP productions which can modulate "slow channel" ion flux and hence slow conducting "slow response" potential activity, could influence patterns of slow conduction in ischaemic myocardium of importance in generating early re-entrant arrhythmias. This possibility has been examined in open chest anaesthetised dogs following experimental coronary occlusion by detailed computer aided analysis and construction of three dimensional maps of regional metabolism, blood flow and epicardial activation patterns at the time of early ventricular arrhythmias. Activation patterns were obtained using an electronic multiplexing system, flow using tracer microspheres and metabolic changes by analysis of multiple tissue samples for lactate and indices of glycolytic activity after rapid excision and freezing of the heart. Marked spacial inhomogeneities in flow, lactate and glycolytic activity were associated with delayed and fragmented activation in the central ischaemic region. Within the border region of flow, however, glycolytic activity was enhanced and conduction generally little impaired. It is suggested that transient changes in the homogeneity of myocardial metabolism and flow are critical in determining patterns of conduction and hence arrhythmogenesis. This may provide a basis for understanding anti-arrhythmic effects of metabolic interventions.

Animals↗
PubMed1981

Lipid lowering and ischaemic heart disease.

There is a non-linear discontinuous relationship between serum cholesterol, and LDL cholesterol, with IHD. There is no sound evidence that reduction of serum cholesterol below 200-210 mg/dl will reduce IHD incidence. It has not yet been shown that regression of advanced lesions in middle-aged men can occur, but regression of cholesterol-induced atheromatous lesions has been achieved in juvenile monkeys by discontinuing atherogenic diets. While the three major primary prevention trials of lowering raised serum cholesterol were all associated with reduction in the non-fatal mortality from IHD--thereby supporting the lipid hypothesis--all also showed an increase in non-cardiovascular mortality. It is legitimate to raise doubts about the consequences on normal biological function of ageing cells of reducing cholesterol concentrations over many years. It is probably of little value to reduce raised serum cholesterol concentrations in patients with overt IHD, since their prognosis is largely determined by the extent of myocardial damage sustained and of coexisting thrombogenic tendency. Patients with familial hypercholesterolaemia should be vigorously treated with a diet with a P/S ratio 1-5, cholestyramine and perhaps nicotinic acid also. The general population should be advised to reduce fat calories to below 30 per cent of total energy with no more than one-third from saturated fat.

Adult↗
PubMed1981

Acute effects of the coronary vasodilator carbocromen on myocardial oxygen consumption, substrate uptake and mechanical performance in intact dogs.

The effects of carbocromen on myocardial substrate uptake, myocardial oxygen consumption (MVO2), and the mechanical activity of the heart was studied in eight intact, anaesthetized dogs. Carbocromen was given i.v. as an injection of 2 mg/kg body weight, and measurements performed in the basal condition and during isoprenaline infusion. Carbocromen increased myocardial blood flow and reduced coronary vascular resistance 15 and 30 min after administration, whereas these values returned to normal after 60 min. The myocardial performance, net myocardial uptake of free fatty acids (FFA), glucose and lactate and MVO2 were not changed by carbocromen. A second isoprenaline infusion 90 min following carbocromen administration induced changes in myocardial performance, net substrate uptake and oxygen consumption not significantly different from isoprenaline infusion prior to carbocromen administration. The antianginal effects by carbocromen observed in clinical studies are more likely to be mediated through its known coronary vasodilator effect than any influence on myocardial metabolism.

Animals↗
PubMed1980

Haemodynamic effects of sulphinpyrazone on exercise responses in normal subjects.

The effects of sulphinpyrazone on heart-rate and blood-pressure responses to exercise were assessed in 15 normal volunteers by a randomised double-blind crossover technique. Submaximal exercise tests were performed 1 and 2 hours after either sulphinpyrazone (SPZ) 200 mg orally or placebo. Heart-rate and blood-pressure responses were unchanged at rest and during exercise 1 hour after SPZ but after 2 hours there was a significant fall in the product of heart-rate and blood-pressure during exercise (peak 35.8 +/- 1.5 x 10(-3) mmHg beats/min, placebo: 33.0 +/- 1.3 x 10(-3) sulphinpyrazone, p < 0.005) and for the first 2 minutes of recovery. This was mainly due to a decreased exercise-induced rise in systolic blood-pressure with lesser effects on heart-rate. This haemodynamic effect of SPZ has a potentially protective oxygen-sparing effect on the normal myocardium during exercise and may explain its apparent benefit in reducing sudden cardiac death after myocardial infarction.

Adult↗
PubMed1979

Effect of myocardial ischaemia and antilipolytic agents on lipolysis and fatty acid metabolism in the in situ dog heart.

Myocardial metabolism was studied in open-chest dogs before and during induction of myocardial ischaemia by coronary artery occlusion. Blood was sampled from a local coronary vein draining ischaemic tissue and from coronary sinus draining predominantly nonischaemic tissue. In the basal state, induction of myocardial ischaemia stimulated myocardial lipolysis as shown by release of glycerol from the ischaemic zone. During isoprenaline infusion, free fatty acids (FFA) extraction across the ischaemic myocardium was substantially increased, but no glycerol release occurred. Pretreatment with nicotinic acid or sodium salicylate markedly depressed FFA extraction across ischaemic myocardium, both during basal and isoprenaline stimulated lipolysis and nicotinic acid most likely inhibited lipolysis in the ischaemic zone. Thus, reduced severity of acute ischaemic injury by antilipolytic treatment might be due to a combination of inhibited myocardial lipolysis and reduced FFA extraction.

Animals↗
PubMed1978

Lack of relation between venous plasma total catecholamine concentrations and ventricular arrhythmias after acute myocardial infarction.

Electrocardiographic tracings were recorded continuously to monitor ventricular tachycardia and R-on-T and R-on-apex-T ventricular premature beats, and repeated estimations of venous plasma total catecholamine concentrations were carried out in 26 patients admitted to a coronary care unit with acute myocardial infarction. No relation existed between the increased catecholamine concentrations found in these patients and the incidence of ventricular arrhythmias occurring six to 48 hours after the onset of symptoms.

Acute Disease↗