Paul Ruegsegger

Fibrinolytic (Plasmin) Therapy of Experimental Coronary Thrombi with Alteration of the Evolution of Myocardial Infarction

To explore the possibilities of fibrinclytic therapy of coronary thrombosis, experimental studies were carried out to document lysis of coronary thrombi and to investigate the effect of fibrinolytic blood upon myocardial infarction. Serum-induced coronary thrombi were produced by a new technic and were followed by serial coronary arteriography. Control animals were compared to animals in which significant fibrinolytic activity had been induced by systemic infusions of plasmin. Tissue studies suggest that plasmin may change the evolution of early infarction. Whether these changes will ultimately result in salvage of ischemic tissue will be determined by studies now in progress.

Salvage of heart muscle by fibrinolytic therapy after experimental coronary occlusion

Abstract 1. 1. The extent of experimental canine myocardial infarction was markedly diminished by fibrinolytic therapy. 2. 2. This effect appeared to be the result of maintaining the patency of the microcirculation of the heart, with the salvage of ischemic marginal areas after coronary occlusion. 3. 3. Fibrinolytic therapy extends the duration of viability of large areas of the myocardium after ischemic injury. 4. 4. Intense fibrinolytic activity was induced to the extent of producing hemorrhagic complications in some of the animals. 5. 5. The implications of this therapy in human myocardial infarction are discussed.

Variations in serum glutamic oxaloacetic transaminase activity in experimental and clinical coronary insufficiency, pericarditis, and pulmonary infarction.

Previous studies have demonstrated consistent rises in serum activity of the enzyme, glutamic oxaloacetic transaminase (SGO-T), following myocardial necrosis of various etiologies. The present study demonstrates markedly different findings in experimental and clinical coronary insufficiency, pericarditis, and pulmonary infarction unless concomitant myocardial necrosis was present. This seems to be a valuable means of differentiating clinical problems in which the presence of myocardial injury is suspected as the basis of the patients chest pain.

Serum Activity Patterns of Glutamic Oxaloacetic Transaminase, Glutamic Pyruvic Transaminase and Lactic Dehydrogenase Following Graded Myocardial Infarction in Dogs

Following experimental myocardial infarction in the dog elevations of serum levels of glutamic-oxaloacetic transaminase (SGO-T), glutamic-pyruvic transaminase (SGP-T) and lactic dehydrogenase (SLD) were consistently noted in decreasing order. Evidence is presented that leakage into the serum from the damaged myocardium plays an important role in these elevations. This concept is supported by analyses of original tissue to blood enzyme concentration gradients, activities of homogenates of infarcts of varying ages, simultaneous measurements of coronary sinus and peripheral venous blood following infarction and contrasting results in man and the dog following infarction.

The electrocardiogram during exercise

Abstract A system is described for recording the electrocardiogram during exercise. This system involves the use of pliable stainless steel mesh electrodes, suitable electrode positioning, recording of the signal on magnetic tape and appropriate filtering. Through the use of these technics, a satisfactory electrocardiographic signal can be obtained during the physical exercises described.

Detection of Hepatitis Carriers by Serum Glutamic Oxalacetic Transaminase Activity

HE REPORTED incidence Of homoloT gous serum hepatitis subsequent to blood transfussion is 0.3 to 1.9% in civilian hospitals1 but was as high as 3.6% in soldiers given blood transfusions in the Korean theater of war.2 By contrast, infectious hepatitis has a reported incidence of about 0.02% An estimated 5 million transfusions are given in the United States each year,3 and, although the total incidence of homologous serum hepatitis is not precisely known, on the basis of the above reports 15,000 to 100,000 cases of homologous serum hepatitis can be expected to develop each year. These patients are, as a rule, out of work for an average of six weeks and 1 to 5 % will die.4