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Biomedical subjects

J E Doherty

Publications and source records attributed to J E Doherty.

At least 55 records · Page 3Linked to original sources
PubMed1978

Ventricular arrhythmias in chronic stable angina pectoris with surgical or medical treatment.

Since both propranolol therapy and saphenous-vein bypass surgery have become accepted treatments for patients with symptomatic coronary-artery disease, it is important to determine if either influences the prevalence of ventricular arrhythmias in these patients. Six-hour dynamic electrocardiography was done on 130 patients with chronic stable angina pectoris at least 1 year after being randomized to surgical or medical therapy. All surgical patients had saphenous-vein grafting; 90% of the medical patients received propranolol. Data analysis showed that even though the overall prevalence of premature ventricular contractions was no different in medical and surgical patients, the prevalence of complex premature ventricular contractions was significantly higher in surgically treated patients not receiving propranolol than in propranolol-treated medical patients (p less than 0.05). However, the survival rate was no different in either group, and the quality of life in the surgical patients remained superior.

Adult↗
PubMed1977

Effect of cholestyramine on digoxin absorption and excretion in man.

Six subjects receiving digoxin therapy for heart disease were studied on two occasions with a single oral dose of 0.5 mg of tritiated digoxin. In every study, all stools and urine were saved for 1 week. Before the second study, treatment with cholestyramine, 4 g every 6 hours, was begun and continued throughout. In three patients, a third study was performed after cholestyramine treatment had been continued for 1 month. Results showed that after cholestyramine administration serum levels, stool output and urinary output of tritiated digoxin varied over a wider range, but cholestyramine had no net short-term effect of any of these variables. After 1 month of cholestyramine administration, there was a small statistically significant increase in stool output of tritiated digoxin and metabolites. In vitro studies suggested that cholestyramine is likely to be a weak digoxin binder in the gut and that changes induced by this resin in digoxin metabolism are not likely to be due to drug binding.

Administration, Oral↗
PubMed1977

Digitalis in pulmonary heart disease (cor pulmonale).

The use of digitalis in pulmonary heart disease has been a topic of great interest for a number of years. The physician's decision to use or not to use digitalis in pulmonary disease has often been an emotional rather than a reasoned one. The diagnostic difficulties from a clinical point of view in separation of pulmonary from cardiac symptoms and findings have also been confusing. The fact that small doses of digitalis may have an inotropic effect on the cardiac muscle has been a difficult concept for many physicians to adopt. On the other hand, the larger doses of digitalis that are often necessary to control the ventricular response in supraventricular arrhythmias sometimes gives rise to confusion. We shall attempt to review the subject in detail and examine indications, contraindications, toxicity, dosage, assessment of benefit, and role of digitalis serum levels in patient management.

Arrhythmias, Cardiac↗
PubMed1977

Pharmacokinetics of digoxin.

The pharmacokinetics of digoxin, the most frequently used digitalis preparation, are reviewed. The dominate serum turnover time is about 34 hours, and is not affected by the route of administration. Excretion is largely as unchanged digoxin in the urine and this excretion is compromised in renal failure. Serum levels of digoxin (determined by radioimmunoassay) are generally available and are useful clinically in assessment of both toxicity and the state of underdigitalization, even though significant overlap exists. Special problems are presented in patients with myocardial infarction, pulmonary heart disease, and thyroid disease.

Acute Kidney Injury↗
PubMed1975

Mitochondrial function, oxygen extraction, epicardial S-T segment changes and tritiated digoxin distribution after reperfusion of ischemic myocardium.

This study examines the effect of 2 hours of reperfusion on transiently ischemic myocardium in pigs. Indexes of myocardial viability measured were mitochondrial function, oxygen extraction, epicardial S-T segment change and distribution of tritiated digoxin. Results were as follows: (1) Mitochondrial function was markedly impaired in the reperfused area after 60 minutes or more of coronary occlusion. The defect would seem to be a block in electron flow near site I, which can be partially bypassed with succinate. (2) An apparent inability of the reperfused myocardium to extract oxygen did not improve with 2 hours of reperfusion. (3) Epicardial S-T segment mapping suggested that necrosis occurred during reperfusion. (4) There was an altered distribution of tritiated digoxin in the reperfused area. The results show that reperfusion for 2 hours did not improve myocardial viability after 60 minutes or more of ischemia.

Adenosine Triphosphate↗
PubMed1975

In-hospital mortality after acute myocardial infarction.

In order to determine if the risk factors contributing to mortality from acute myocardial infarction (MI) during the period of coronary care unit (CCU) observation are different from those in patients dying in the hospital after CCU discharge, the hospital records of 172 acute MI patients seen over an 18-month period were reviewed. Of the 32 deaths from acute MI, 25 per cent occurred suddenly outside the CCU. The risk factors identified in the 32 deaths were (1) anterior MI (2) Previous MI, (3) cardiac failure, (4) significant ventricular arrhythmia, (5) intraventricular conduction defects, and (6) murmur suggestive of papillary muscle dysfunction. These same risk factors were found to be far more frequent in the patients dying suddenly outside the CCU.

Adult↗
PubMed1975

Tritiated digoxin: studies in renal disease in human subjects.

Digoxin is excreted primarily in the urine as the unchanged glycoside: 60-80% can be recovered from the urine in 7 days after a single intravenous dose in the human subject. Definition of the role of the kidney in digoxin excretion, turnover and metabolism was studied in 57 patients with renal disease, transplant candidates and/or donors and recipients of renal transplants. A single dose of 3H digoxin was given to the subjects, frequent serum samples were obtained and all urine and stools were saved for 7 days. All specimens were extracted with chloroform and digoxin, and its metabolites were separated by column chromatography. Results reveal that the serum T1/2 and the dominant T1/2 of digoxin are prolonged in renal disease in direct proportion to the reduction in creatinine clearance (r = 0.833). The blood urea nitrogen (BUN) is also related to digoxin clearance (r = 0.742). The higher the BUN, the less digoxin excreted in the urine. Anephric patients excrete more digoxin in stool, but this does not compensate for the lack of renal excretion. Transplanted kidneys excrete digoxin in proportion to renal functional capacity, as do patients who have experienced unilateral nephrectomy. Peritoneal or hemodialysis is not effective in removing digoxin from the human subject and may lead to digitalis intoxication if K+ is allowed to fall to critical levels. Digoxin excretion is not volume related, as patients with nephritogenic diabetes insipidus excrete the drug normally with urine volumes of 12 liters a day. Digoxin doses in renal insufficiency should be dictated by knowledge of renal functional ability of the kidneys and after "normal" loading doses, and maintenance doses should be 1/4 to 1/2 those usually administered.

Adult↗
PubMed1975

Impairment of mitochondrial function following reperfusion of acutely ischemic myocardium.

This study examines indices of respiratory function in mitochondria prepared from transiently ischemic myocardium that had been reperfused in order to evaluate the validity of performing early surgical revascularization procedures. Experiments were performed in pigs with temporary ligation (15-80 min) of an anterior descending coronary artery followed by a 2-hr reperfusion period. Mitochondria preparations were studied simultaneously from normal and reperfused mitochondria in malate and glutamate substrates using the polarographic method. Results revealed a marked decrease of oxygen consumption of mitochondria from reperfused myocardium with relative preservation of oxidative phosphorylation (near normal ADP/O ratio). These results are compatible with a block in electron transport, a theory which was further supported by the data obtained using dinitrophenol as an uncoupler. Additional studies suggested the block was located at site I in the electron transport chain since mitochondrial oxygen consumption, including ATP-linked oxygen consumption, was enhanced by the use of succinate in combination with glutamate. The abnormal mitochondrial function observed is probably due to ischemia persisting despite reperfusion.

Acute Disease↗