Renal Micropuncture Study of the Development of Anuria in the Rat with Mercury-induced Acute Renal Failure*

Abstract

Acute renal failure in man may result from such factors as trauma, transfusion accidents, sepsis, burns, and acute poisoning with carbon tetrachloride, ethylene glycol, or mercury. Regardless of the etiology and despite marked variability in the histologic appearance of the kidneys of individual cases, most patients with acute renal failure develop oliguria or anuria together with evidence of impaired tubular function. The cause of this decrease in urine volume, however, has not been well defined. Some theories commonly conjured to explain the oliguria of acute renal insufficiency stem largely from pathological findings rather than from functional studies in vivo. Of these findings, three have been stressed as possibly being responsible for oliguria: tubular obstruction by cellular debris (1-3), tubular compression by interstitial edema (4-7), and "passive backflow" of glomerular filtrate through holes in the wall of the tubule (6,8,9). We have attempted to determine the possible role of these factors in mercury-induced acute renal failure in the rat. perimentation. Their food and fluid intake and urine volume were measured; animals whose water intake was less than 10 ml during this period received supplementary fluids intraperitoneally in the form of 75 mM saline. Mercuric chloride, 12 mg per ml 140 mM NaCi, was injected intramuscularly at a dose of 12 mg per kg, control animals receiving a comparable volume of saline alone. Micropuncture experiments were performed at times ranging from 2 to 27 hours after mercury injection, and the fluid intake and output in the intervening period were recorded. Urine osmolalities, measured cryoscopically with a Fiske osmometer, were obtained routinely in early experiments to rule out hypovolemia due to a redistribution of body water and a resultant ADH effect as the sole cause of oliguria. Since urine osmolalities in mercury-treated animals were consistently less than 610 mOsm per kg, these measurements later were discontinued. MethodsAnimals were anesthetized with sodium pentobarbital, 35 mg per kg body weight, supplementary pentobarbital being added as necessary. They were placed supine and warmed from above with an infrared lamp to maintain body temperature at 400 C. The left kidney was exposed through an abdominal-flank incision and gently dissected from the perirenal fat. The renal capsule was left intact, but in dissecting the kidney from its bed collateral circulation through capsular vessels was virtually abolished. The kidney was placed in a Lucite holder as gently as possible, care being taken to avoid distortion of the renal vessels and ureter. The surface of the kidney was illuminated with a 25-w zirconium arc lamp and covered with warm mineral oil to prevent surface evaporation and facilitate visualization of the renal architecture. The blood pressure of each animal was monitored with either a tail microphone apparatus or direct aortic manometry. When the tail microphone was used, a 1-cm occluding cuff was placed at the base of the tail and the pickup positioned ...

An inhibitory effect of furosemide on sodium reabsorption by the proximal tubule of the rat nephron

“…Experimental kidney GFR fell, on the average, by 15% (from 0.96 to 0.80 ml/min) after furosemide administration. The values for nephron GFR observed in control and experimental rats were similar (Table II) and agree closely with values reported by others for comparably hydrated animals (16,17). It should be noted that in these antidiuretic animals the variability in this measurement was considerable.…”

The relationship between glomerular filtration rate and sodium reabsorption by the proximal tubule of the rat nephron

“…The mean nephron GFR during the recollection period in control animals was very nearly the same as the mean value during the initial collection (Table II). These mean values do not differ significantly from the mean value obtained during the unclamped period in the slow infusion experimental group and are similar to values reported by others (5,9,16). The mean nephron GFR in the absence of clamping in the moderate infusion group was about 20% higher, presumably reflecting the effect of extracellular fluid (ECF) volume expansion.…”

The Renal Lesion Associated with Hemoglobinemia: A Study of the Pathogenesis of the Excretory Defect in the Rat*

“…The precise alterations in discrete renal functions that lead to the excretory failure characteristic of this syndrome remain unknown. However, knowl-edge in this area is advancing as refined techniques are applied to the study of lesions induced in experimental animals, which may be analogous to those occurring in man (1)(2)(3). The present study deals with an attempt to produce such a model by inducing acute renal failure associated with hemoglobinemia in the rat.…”