The appearance of proteinuria in patients suffering from congestive heart failure is a common clinical occurrence. Since such patients, without any intrinsic renal disease, frequently have both an elevated renal venous pressure and a reduced renal blood flow (1), it would seem that either one or both of these factors may lead to proteinuria.Proteinuria has been produced experimentally by partial obstruction either of the renal artery or of the renal vein (2-5). In most of this work, however, studies of renal hemodynamics were incomplete, or when adequate pressure and blood flow measurements were made (6, 7), the experiments were such that it was impossible to determine specifically which hemodynamic factor was responsible for the appearance of the proteinuria.The present study was The estimations of renal plasma flow (RPF) and glomerular filtration rate (GFR) for each kidney were made by determining the clearances of para-aminohippurate (PAH) and exogenous creatinine, respectively. Blood samples were drawn at the midpoint of each clearance period from the right femoral artery through an indwelling needle. During the operative procedure the animal was given intravenously a priming d.nse of 1.5 grams of creatinine dissolved in 30 ml. of water. This was followed by a sustaining infusion of an 0.85 per cent NaCl solution delivered at a constant rate of 3 or 5 ml. per minute by a Bowman Pump for the remainder of the experiment. This sustaining infusion contained sufficient amoants of creatinine and PAH so that these substances were delivered at rates of 20 mg. of creatinine per minute and 3 mg. of PAH per minute. In some instances an additional infusion of NaCl solution (0.85 or 1.5 per cent) was given during the course of the experiment. The reason for this will be discussed later.After completion of the operative procedure the animal was allowed to recover for about 30 minutes. One or more control urine samples were then collected in order to measure the clearances and determine the presence of proteinuria. The clamp was then tightened until the pressure in the left renal vein rose to the desired level. After the pressure had been elevated for 15 to 30 minutes, con-secutive urine samples were collected until proteinuria appeared or until the pressure had been elevated for 1 to approximately 3 hours without the occurrence of proteinuria. The clamp was then released allowing the pressure in the left renal vein to fall freely.After an interval of time at least sufficient to allow the renal dead space to be cleared, one or more recovery samples were collected.Creatinine concentration in urine and plasma was determined by the method of Kennedy, Hilton, and Berliner (9). PAH concentration in urine and plasma was determined by the method of Smith, Finkelstein, Aliminosa, Crawford, and Graber (10).The method used to determine the concentration of protein in urine was a modification of the method of 737

Most investigators are agreed that acute and chronic arteriovenous fistulae produce an increase in cardiac output (1, 2). Furthermore, a chronic fistula of sufficient size produces an increase of the blood volume (1, 2) and, upon closure of such a chronic fistula, a diuresis of sodium and water (3). On the other hand, it has been shown recently that an acute arteriovenous fistula accommodating 20 per cent or more of the original cardiac output increases the cardiac output but leads to a decrease in the blood flow through the normal systemic capillary bed due to vasoconstriction (1). It appeared of interest, therefore, to determine whether the renal vascular bed participates in this vasoconstriction and, if so, whether an acute arteriovenous fistula affects the renal functions in such a manner as to result in sodium and water retention. METHODSTen adult female dogs were anesthetized by the intravenous administration of 0.47 to 0.57 cc. per kilogram of a 6 per cent solution of sodium pentobarbital. The trachea was cannulated with a Y-shaped glass tube. Segments of the right common carotid and right brachial arteries, right jugular vein, as well as both femoral arteries and veins were dissected free. After the necessary dissection was completed, a multi-eyed catheter was introduced into the urinary bladder. The animal was then given intravenously 5 to 10 mg. of heparin per kilogram after which the vessel cannulations and the other necessary procedures were carried out as described below. The mean arterial blood pressure was recorded with a mercury manometer connected to the central end of the left femoral artery. In 3 of the 10 experiments, the cardiac output was measured according to the Fick prin-

By means of venous occlusion digital plethysmography, the authors have evaluated the peripheral vasodilating effect on normal and diseased arterioles of a new adrenergic blocking agent, Regitine, 2-[-( m -Hydroxy-N- p -tolylanilino)-methyl]-2-imidazoline. Results have been compared with the results of similar studies using Priscoline and indirect body heating to produce vasodilation. The effect of palrenteral Regitine on pulse and blood pressure has been noted as well as the clinical results obtained when this drug was used orally for the treatment of certain forms of peripheral vascular disease.

Background: Immunotherapy (IOT) of cancer depends on intratumoral CD8+ cells that can overcome multiple obstacles to their localization and function. CD8+ cell content and its changes with treatment are important to understand tumor immunobiology, prognosis, and to guide therapy.