Abstract
The rate of rise of blood urea nitrogen (BUN) in acute renal failure in man is extremely variable. This has been attributed to varyingly increased rates of urea production in the presence of tissue catabolism due to infection, trauma, or operative intervention. Some degree of metabolic acidosis is an almost invariable accompaniment of acute renal failure and the effects of the acidosis on the rate of rise in BUN have not received attention. This communication reports a study of acute renal failure in the rat, in which it was possible to demonstrate that correction of acidosis per se significantly diminished the rate of rise of the blood urea nitrogen.
Materials and Methods. Male Sprague-Dawley rats, weighing 180 to 280 g, were fasted but allowed free access to water for 16 hr prior to surgery. They were then anesthe-sized with pentobarbital (5 mg/100 g ip) and subjected to either bilateral ureteral ligation or sham operation. Bilateral ureteral ligation was carried out through separate dorsal incisions. Sham operation consisted of mobilization and preparation of both kidneys for ureteral ligation. During the 48-hr postoperative period food and water were withheld and each rat was kept in an individual metabolic cage in a room at constant temperature. One group (9 animals) of the ureter-ligated animals received no further treatment, a second group (6 animals) was given 0.75 mEq of NaHCO3 in 5 ml of water ip at 20 and 40 hr after surgery and a third group (6 animals) was given 0.75 mEq of NaCl in 5 ml of water, also at 20 and 40 hr after surgery. At 48 hr postoperatively all rats were again anesthesized with pentobarbital (5 mg/100 g ip) and blood was obtained from the aorta in a heparinized syringe for determination of arterial pH by the micro Astrup apparatus (Radiometer, Copenhagen) and for BUN by the method of Crocker (1). PH units were converted into hydrogen ion concentration (nEq/liter) before the data were analyzed statistically by analysis of variance (2).
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