Thesis (Ph. D.)--University of Wisconsin--Madison, 1985. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 178-200).

The purpose of this study was to examine exercise responses during acute and chronic administration of BB, Beta Blockade. Twenty-eight healthy males performed maximal treadmill exercise tests after 1 day and 9 days of 3 double-blind, randomized conditions: a placebo (Pl), propanolol (Pr) 80 mg bid, and atenolol (At) 100 mg daily. Maximal heart rate (HR), oxygen consumption (VO₂), ventilation (VE), and treadmill time (TT) were significantly reduced by Pr and At after an acute and chronic dose. An acute dose of Pr and At caused a greater decrease in maximal HR compared to chronic administration (143.1 ± 5.0 b min⁻¹ at day 1 vs. 147.7 ± 4.2 b min⁻¹ at day 9). However, the overall exercise response was not effected by the change in HR in either the TR or UT subjects. These data indicate that there is no difference in exercise response to acute and chronic BB in young healthy males. (Abstract shortened with permission of author.)

Thesis (M.S.)--University of Wisconsin--Madison, 1984. / Typescript. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 81-86).

Two investigations were conducted to examine the influence of beta-adrenergic blockade on cardiovascular, respiratory, metabolic, and thermoregulatory responses to maximal and submaximal exercise in both highly trained and untrained subjects. In both studies, subjects received randomized and double-blind oral medication with atenolol (100 mg/day), propranolol (160 mg/day), and placebo. In the first study significant reductions in HR max and ‘VO₂ max resulted during the atenolol and propranolol treatments in both the trained and untrained subjects. However, the reductions in ‘VO₂ max were significantly greater in the trained subjects and both groups experienced their greatest reduction during the propranolol treatment. In all subjects, the magnitude of reduction in HR max was significantly greater than the concomitant decrease in ‘VO₂ max. It is concluded that untrained subjects have a greater compensatory reserve than do trained subjects during maximal exercise while under beta-adrenergic blockade. In addition, significant advantages were found with the use of a selective compared to a non-selective beta blocker. Thermoregulation during prolonged exercise in the heat with beta blockade was studied in fourteen subjects. Subjects performed 90-minute cycle ergometer rides at a workload equivalent to 40% of the subjects' unblocked ‘VO₂ max. Rectal temperature was slightly higher during the atenolol trial compared to the placebo but was not different during the propranolol trial compared to the placebo. Skin blood flow was significantly lower during the propranolol trial compared to both the atenolol and placebo trials, but it did not differ significantly between the atenolol and placebo trials. Maintenance of rectal temperatures appeared to be achieved through changes in sweat rate, skin blood flow, and a reduced heat production, i.e., lower ‘VO₂ during the propranolol trial. The decrease in cutaneous blood flow reported during the propranolol trial is likely associated with the associated increase in TPR. This increase in TPR would help to compensate for the lower ‘Q and, hence, help maintain mean arterial pressure. Changes in substrate utilization, i.e., decreased lipolysis, during the beta-blocked trials may also be indicated. Lastly, the inability of two subjects to complete the 90-minute ride, the elevated RPE values, and the additional side effects reported during the propranolol trial would indicate an advantage for the use of a selective blocker.

Thesis--M.D., University of Hong Kong, 1982.

No description available.

This thesis is concerned with the influence of acute and long-term beta-adrenergic blockade on myocardial infarction in man. An original statistical evaluation of all published and some available unpublished clinical trials is presented in Chapter I. Chapter III and TV concern the measurement and evolution of infarct size in man. In Chapter III, praecordial ECG mapping and the standard 12 lead ECG have been correlated with cumulative release of the MB isomer of creatine kinase. Using these techniques, I have found that approximately 50% of eventual infarction is complete in 6 hours; implying that interventions designed to salvage ischaemic myocardium may be feasable (Chapter IV). In Chapter V, I have demonstrated delayed beta-adrenergic blockade after oral administration of atenolol and that an initial intravenous dose is essential to achieve early and effective beta-blockade. In a randomised control trial of 215 patients, atenolol administered intravenously within 12 hours of pain, prevented infarction in treated patients with initial threatened infarcts and reduced infarct size and morbidity in those with initial definite infarcts (Chapter VI). Patients with anterior myocardial infarction, randomised to receive atenolol for a year, showed significantly greater R wave recovery and Q wave disappearance on serial praecordial maps compared to placebo patients. In a further study, this was demonstrated to be due to lowering the heart rate. This phenomenon of improved EGG recovery with atenolol was reproduced in experimental infarction and was shown to be due to improved scar shrinkage (Chapter VII). The implications of these studies are discussed. It is likely that both early and long-term beta-blockade will be beneficial to patients with myocardial infarction.

Thesis (M.S.)--University of Toledo, 2009. / Typescript. "Submitted as partial fulfillment of the requirements for the Master of Science Degree in Medicinal Chemistry." "A thesis entitled"--at head of title. Bibliography: leaves 45-48.

Thesis (M.D.)--University of Hong Kong, 1982. / Also available in print.

No description available.