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Biomedical subjects

L H Opie

Publications and source records attributed to L H Opie.

At least 19 recordsLinked to original sources
PubMed1979

Catecholamine-mediated arrhythmias in acute myocardial infarction. Experimental evidence and role of beta-adrenoceptor blockade.

Ventricular fibrillation is a major mechanism of sudden death. The cellular link between catecholamine activity and the development of serious ventricular arrhythmias may be in the formation of cyclic adenosine monophosphate (cAMP). Cyclic AMP and agents promoting cAMP accumulation allow development of slow responses which, especially in the presence of regional ischaemia, could develop into ventricular fibrillation. The role of beta-antagonist agents in the therapy of acute myocardial infarction is analysed in relation to the hypothesis linking cAMP and ventricular fibrillation. Reasons for the limited effectiveness of anti-arrhythmic therapy with beta-antagonist agents are given.

Adrenergic beta-Antagonists↗
PubMed1979

The heart in diabetes mellitus. Part I. Biochemical basis for myocardial dysfunction.

The heart in acutely diabetic animals is subject to multiple inhibitions of glucose metabolism caused by enhanced metabolism of free fatty acids (FFA) and ketone bodies. Such metabolic changes may impair the reaction of the diabetic heart to oxygen lack. In chronically diabetic hearts the increased deposition of triglycerides in the heart and the formation of glycoproteins may underlie the newly recognized clinical entity of diabetic cardiomyopathy.

Alcoholism↗
PubMed1979

Does cimetidine alter the cardiac response to exercise and propranolol?

The recent discovery of histamine (H) receptors in the heart raises the possibility that the H2-antagonist drug, cimetidine, used in the therapy of peptic ulcer, might have cardiac side-effects and might impair the cardiac response to exercise. In 10 normal subjects, cimetidine did not alter the normal heart rate and blood pressure response to treadmill exercise, nor was the effect of beta-blockade by propranolol exaggerated. Thus it appears that the use of propranolol is not necessarily a contraindication to cimetidine therapy, or vice versa. However, further trials on patients with ischaemic heart disease are required to exclude any additive effects of cimetidine and propranolol on the diseased heart.

Adult↗
PubMed1979

Protective action of amiodarone against ventricular fibrillation in the isolated perfused rat heart.

The pretreatment of rats with amiodarone for 2 minutes to 3 weeks before the excision of their hearts caused a dose-related decrease in heart rate and an increase in the ventricular fibrillation threshold both before and after coronary arterial ligation. Similarly, amiodarone decreased the incidence of ventricular premature extrasystoles, ventricular tachycardia and fibrillation during the period of regional ischemia after coronary arterial ligation and also after reperfusion of the ischemic myocardium. There was no evidence of a metabolic protective effect on ischemic myocardium because tissue high energy phosphate content decreased to a similar extent in ischemic myocardium from control and amiodarone-treated rats. Instead, the protective effect of amiodarone against fibrillation was accompanied by attenuation of the increase in tissue cyclic adenosine monophosphate in ischemic myocardium after coronary arterial ligation. It is proposed that amiodarone exerts a potent antifibrillatory effect by decreasing tissue cyclic adenosine monophosphate in ischemic myocardium.

Amiodarone↗
PubMed1979

Role of glycolytic flux in effect of glucose in decreasing fatty-acid-induced release of lactate dehydrogenase from isolated coronary ligated rat heart.

The mechanisms whereby glucose reduces fatty acid-induced release of enzyme from the coronary-ligated isolated perfused working rat heart are investigated. Alterations in the tissue contents of ATP, phosphocreatine, or glycogen could be excluded as possible mechanisms for the beneficial effect of glucose in this system. Provision of glycolytic ATP from increased glycolytic flux may be one important factor.

Adenosine Triphosphate↗
PubMed1979

Hypertrophic cardiomyopathy associated with sudden death during marathon racing.

An experienced marathon runner died suddenly during a competitive race. At necropsy, ventricular hypertrophy but no asymmetrical septal hypertrophy was found. Histological studies showed features of hypertrophic cardiomyopathy. The coronary arteries were normal. We propose that the runner died from myocardial ischaemia, precipitated by marathon running on a background of hypertrophic cardiomyopathy. Excess cardiac work, induced by marathon running in the presence of mild congenital cardiac defects, could have contributed to the development of the cardiomyopathy.

Adult↗