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-