Walter E. Judson
Boston University
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Featured researches published by Walter E. Judson.
Circulation | 1956
Walter E. Judson; William Hollander; Robert W. Wilkins
Intravenous Apresoline is a powerful renal vasodilator in cardiac as well as in noncardiac patients. In hypertensive patients in congestive heart failure, the drug produces a striking improvement in both cardiovascular and renal function. The increases in renal plasma flow are inconsistently related to changes in arterial pressure and cardiac output Unlike many hypotensive drugs, Apresoline usually causes no decrease in the renal excretion of sodium and water. Circulatory collapse produced by the drug may occur in the presence of an increased cardiac output but is accompanied by a deterioration of the arterial pressure pulse and a reduction in sodium and water excretion.
Circulation | 1955
Paul Stucki; J. D. Hatcher; Walter E. Judson; Robert W. Wilkins
Circulation times (P32 from the antecubital and femoral veins to a peripheral artery) and roentgenographic studies of the pattern of venous distribution of a radio-opaque substance (Diodrast introduced through a cardiac catheter into the axillary vein and the inferior vena cava below the diaphragm) have been performed during the expiratory effort of the Valsalva maneuver. In normal subjects the circulation times were increased by the duration of the expiratory effort and the Diodrast injections were stagnated in the veins outside the thoracic cavity. These effects were in striking contrast to those in patients with congestive failure in whom the circulation times were retarded only partially if at all and the Diodrast injections continued to flow freely towards the right atrium during the expiratory effort. Thus, in patients with congestive failure the Valsalva maneuver does not interrupt the venous return to the right atrium as it does in normal subjects.
The New England Journal of Medicine | 1954
Robert W. Wilkins; Walter E. Judson; Richard W. Stone; William Hollander; William E. Huckabee; Irwin H. Friedman
RECENTLY, Rauwolfia serpentina was introduced into this country for the treatment of hypertension.1 2 3 This stimulated renewed chemical and pharmacologic studies on the drug, which had been known ...
Circulation | 1958
William Hollander; Walter E. Judson
The increased capacity of hypertensive subjects to excrete sodium is frequently reduced by effective antihypertensive drug treatment. This reduction in sodium excretion is not necessarily associated with changes in renal hemodynamic function or resting sodium excretion. It appears to result from an alteration in renal tubular activity. The findings suggest that the arterial pressure per se may operate to control sodium excretion. They also are consistent with the hypothesis that certain disturbances in sodium excretion in arterial hypertension may be the result and not necessarily the cause of an elevated blood pressure.
Circulation | 1956
Walter E. Judson; William Hollander; Robert W. Wilkins
Antihypertensive drug treatment is capable of aggravating angina pectoris in hypertensive patients with coronary artery disease. The complication appears to be due to different hemodynamic mechanisms. Angina pectoris caused by hydralazine may result not only from a reduction in aortic perfusion pressure but also from increases in cardiac output and pulse rate which the drug produces. Coronary insufficiency, after the administration of hexamethonium, is usually associated with severe hypotension and results primarily from a reduction in aortic perfusion pressure. Hexamethonium was not found to prevent the anginal effects of hydralazine. Intravenous hydralazine is a sensitive test for coronary insufficiency but is not without untoward reactions.
Journal of Clinical Investigation | 1955
Walter E. Judson; J. D. Hatcher; William Hollander; Meyer H. Halperin
The effects of mitral valvuloplasty on general cardiohemodynamic function in patients with mitral stenosis have been reported by many investigators (1-10). Measurements of renal blood flow, glomerular filtration rate, and excretion of sodium and their correlation with changes in cardiac output, blood oxygen measurements, and vascular pressures also have been extensively studied in patients with various types of heart disease, with and without congestive failure, at rest (11, 12) and during exercise (13-15). However, little information is available on the changes in renal circulation or excretion of electrolytes and water in the period early after mitral valvuloplasty (16). The purpose of this paper is to describe these changes in renal function and to correlate them with alterations in cardiovascular responses. Particular effort has been made to determine whether a specific cardiohemodynamic pattern is associated with disturbances of salt and water excretion before and after mitral valvuloplasty, both at rest and during exercise.
The New England Journal of Medicine | 1953
Robert W. Wilkins; Walter E. Judson
Journal of Clinical Investigation | 1958
William E. Huckabee; Walter E. Judson
Circulation | 1955
Walter E. Judson; J. D. Hatcher; Robert W. Wilkins
Journal of Clinical Investigation | 1955
Walter E. Judson; William Hollander; J. D. Hatcher; Meyer H. Halperin; Irwin H. Friedman