Far sighted plan bears fruit.
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Biomedical subjects
Publications and source records attributed to M Thomas.
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Propranolol is known to decrease ischaemic damage in developing myocardial infarction. Besides acting on mechanical parameters which help determine the balance of oxygen supply and oxygen demand in the ischaemic tissue, propranolol decreases the myocardial uptake of free fatty acids and increases that of glucose. It is suggested that propranolol may favourably alter developing myocardial infarction in dogs by altering the supply of substrates reaching the ischaemic zone. However, propranolol also decreases enzyme release from isolated rat hearts with coronary ligation at a relative constant arterial free fatty acid concentration. Propranolol causes more marked depression of mechanical function and of heart rate in hearts perfused with free fatty acids than with glucose. It is suggested that the glucose-promoting and anti-lipolytic actions of propranool might be important not only in decreasing infarct size but also in helping to prevent undesirable side effects in hearts with experimental myocardial infarction.
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Serum digoxin level was determined by radioimmunoassay in 76 elderly in-patients (age: 76.1 +/- 1.0) which were treated by digoxin without any evidence of toxicity. Digoxin levels was related to blood nitrogen (p less than 0,01); on the other hand, no relationship between others factors influencing the digoxin bioavailability (age, body weight, associated drug) and digoxin levels could be found. Therapeutic effectiveness, as estimated by ventricular rate and signs and symptoms, was not dependent of digoxin levels. In patients with higher functional class (III and IV NYHA), however, digoxin level was generally demonstrated to be increased. Digoxin levels were lower in patients with coronary heart disease (1.71 +/- 0,22 ng/ml; n = 16) than in patients with right ventricle overload (2.94 +/- 0,74 mg/ml; n + 7 - p less than 0.05). Because of the very large scattering of digoxin levels, digoxin determination seems to be useful in measuring individual bioavailability and therapeutic effectiveness, and leading to the best base line of any individual treatment.
It is generally accepted that ST segment elevation is one of the characteristic electrocardiographic features of acute myocardial infarction. In experimental myocardial infarction the degree of ST segment elevation has been related to the degree of change in coronary flow. Surface mapping in patients of the electrocardiographic potentials gives an indirect representation of the epicardial ST segment change and in indication of the area of underlying myocardial damage. A number of patients who had sustained myocardial infar-tion within 72 hours were studied. All the patients had a history of prolonged ischaemic cardiac pain, electrocardiographic changes and a rise in serum enzymes. Electrocardiagrams were recorded from 72 points on the chest surface. Control maps were constructed from the ST segment changes measured at each of these points and plotted on a standard diagram. Electrocardiograms were recorded during a control period immediately before 20 mg of practolol was given intravenously over a period of five minutes. In all patients practolol produced a significant reduction in the area of ST segment elevation as represented by a reduction in the number of points with ST elevation of more than 2 mm. The significance of these findings is discussed.
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