PubMed Health⌕ Search

Biomedical subjects

B J Stinebaugh

Publications and source records attributed to B J Stinebaugh.

At least 19 recordsLinked to original sources
PubMed1990

Removal of an inorganic acid load in subjects with ketoacidosis of chronic fasting.

When a large inorganic acid load is ingested by normals, the proton load is eliminated because the rate of excretion of ammonium can rise to 200 to 300 mmol/day. In subjects with ketoacidosis of chronic fasting, such a large increase in the rate of excretion of ammonium might not be possible because of ATP balance considerations in proximal cells. Subjects with ketoacidosis of chronic fasting excreted less net acid as defined in the conventional way when they consumed a large inorganic acid load (136 +/- 6 vs. 176 +/- 26 mmol/day in control fasted subjects). Nevertheless, the vast majority of this inorganic acid load was eliminated because they were in steady state and had only a slightly lower concentration of bicarbonate (13 +/- 0.6 vs. 15 +/- 0.5 mmol/liter) and ketoacid anions (3.3 +/- 0.2 vs. 5.5 +/- 0.2 mmol/liter) in their blood. Using a definition of net acid excretion where the component of bicarbonate loss was expanded to include "potential bicarbonate" (ketoacid anions) in the urine, the rate of excretion of net acid was higher in subjects who ingested the inorganic acid load, owing to a much lower rate of excretion of ketoacid anions (9 +/- 2 vs. 120 +/- 7 mmol/day). This lower rate of excretion was not only due to a lower filtered load, but also to a higher fractional reabsorption of ketoacid anions during acidosis (97 +/- 0.1 vs. 77 +/- 0.2%). This higher fractional reabsorption could not be explained by a lower filtered load of ketoacid anions or to a restricted intake of sodium.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1985

Distal renal tubular acidosis syndromes: a pathophysiological approach.

Ammonium is the most important component of renal acid excretion. A reduced rate of ammonium excretion is the common feature of the group of diseases called distal renal tubular acidosis. We have presented an alternative approach to patients with distal acidification defects based upon the pathophysiology of these disorders. Accordingly, the purpose of this review is to describe a revised classification based on our current understanding of collecting duct hydrogen ion secretion and ammonium addition to the lumen of the distal nephron. We have subdivided these defects into four groups: disorders of the collecting duct proton pump (pump defects); failure to generate and/or maintain an appropriate electrical gradient to favor hydrogen ion secretion (voltage defects); back-leak of hydrogen ions across an abnormally permeable collecting duct membrane (gradient defects), and diminished availability of NH3 in this nephron segment (NH3 defects). These four subtypes can be identified by measuring the urine pH and PCO2 under appropriate circumstances and evaluating the renal excretion of ammonium and potassium.

Acidosis, Renal Tubular↗
PubMed1984

The effect of hypocalcemia on renal bicarbonate absorption.

The effect of hypocalcemia on renal bicarbonate absorption (RHCO3/GFR) was examined in bicarbonate-loaded dogs. Following the infusion of ethylene-bis(oxyethylenitrilo)tetraacetic acid (EGTA) in intact dogs, RHCO3/GFR fell from 23.8 +/- 0.7 to 20.8 +/- 0.6 (p less than 0.005) and in thyroparathyroidectomized (TPTX) dogs from 25.6 +/- 1.44 to 23.6 +/- 2.15 (p less than 0.025). By contrast, infusion of EGTA which had been titrated with calcium had no effect, RHCO3/GFR being 27.7 +/- 1.14, control and 28.5 +/- 0.38, during EGTA (p less than 0.05). Hypocalcemia also significantly depressed the renal absorption of phosphate. There were no effects on renal hemodynamics or electrolyte excretion. These studies suggest that plasma-ionized calcium may play a role in regulating renal bicarbonate and phosphate absorption.

Animals↗
PubMed1983

Decreased distal acidification in acute hypercapnia in the dog.

The present studies evaluate the effect of acute hypercapnia on distal nephron H+ secretion (DNH+S) in vivo by means of the urine-blood PCO2 difference (U-B PCO2) in alkaline urine. Bicarbonaturia was induced by either a sodium bicarbonate infusion or L-lysine administration. Our results demonstrate that the U-B PCO2, as a function of the urinary bicarbonate concentration, was significantly lower during acute respiratory acidosis; this effect was not dependent on changes in glomerular filtration rate and/or fractional excretion of sodium, potassium, and chloride. Infusion of the sodium salts of sulfate, a nonreabsorbable anion, did not correct the diminished U-B PCO2. Amiloride caused the U-B PCO2 to fall in normocapnic dogs but not in hypercapnic dogs. When hypercapnia was superimposed in dogs with extracellular fluid volume contraction, there were no changes in the U-B PCO2. This study indicates that acute hypercapnia in the intact dog decreases DNH+S and is compatible with an effect of hypercapnia on the voltage-dependent component of urine acidification. The mechanism appears to be direct rather than secondary to factors that influence the rate of sodium delivery to the distal nephron.

Acidosis, Respiratory↗
PubMed1981

Evaluation of the effect of pentobarbitone anaesthesia on the plasma potassium concentration in the rabbit and the dog.

The purpose of these studies was to determine the reasons for the hypokalaemia observed in rabbits studied in our laboratory. The rabbits consumed standard rabbit chow which is rich in potassium and remained in potassium balance. Hypokalaemia was only observed following anaesthesia. A number of additional investigations were undertaken to clarify the mechanisms involved. The hypokalaemia could not be attributed to technical factors, alkalaemia, hyperinsulinaemia or hyperaldosteronism, but seemed to be a function of anaesthesia. This effect of pentobarbitone anaesthesia was not unique to the rabbit, as similar changes also occurred in the anaesthetized dog. The findings reported in this paper have significant implications with respect to the interpretation of plasma potassium concentrations in anaesthetized subjects or animals.

Acid-Base Equilibrium↗
PubMed1981

Sites of ammonia addition to tubular fluid in rats with chronic metabolic acidosis.

The purpose of this investigation was to determine in which nephron segments ammonia was added to or removed from the lumenal fluid of the rat. Ammonium was measured in proximal and distal tubular fluid samples obtained by micropuncture and in collecting duct fluid samples obtained by microcatheterization. Water abstraction was assessed by examining the tubular fluid-to-plasma inulin concentration, (TF/P)In. In normal or acidotic rats, the vast bulk of the final urine ammonium appeared in the proximal tubular fluid samples. Most of this ammonia was lost, however, in transit from the proximal to the distal tubule so that only 20 to 30% of the excreted ammonium was present at the distal site. Ammonia reentered the lumenal fluid primarily in the cortical collecting duct in acidotic rats and in the medullary collecting duct in normal rats. Although the pattern was qualitatively similar in both groups of rats, the absolute quantity of ammonium in each nephron segment of normal rats was about 10 to 20% of that in acidotic animals.

Acidosis, Renal Tubular↗
PubMed1981

Ammonia addition into the medullary collecting duct of the rat.

The purpose of these studies was to determine if ammonia is added directly to the medullary collecting duct of the rat, and if so, to estimate its quantitative contribution to ammonium excretion. Samples of fluid were obtained along the length of the medullary collecting duct by retrograde microcatheterization. To document net addition of ammonium, we measured the ammonium concentration in tubular fluid by an enzymatic isotope technique, and we calculated the degree of fluid reabsorption from the ratio of the inulin concentration in tubular fluid and plasma. The ammonium concentration corrected for water reabsorption ([NH4+]/[TF/P]In) rose progressively from the beginning to the end of the medullary collecting duct, indicating net ammonia addition to this nephron segment. By calculation, it appears that about 40% of the excreted ammonium reached the urine by direct addition of ammonia to the duct fluid.

Ammonia↗
PubMed1981

Studies on the regulation of hydrogen ion secretion in the collecting duct in vivo: evaluation of factors that influence the urine minus blood PCO2 difference.

The purpose of these studies was to clarify the basis of the relationship between the urine bicarbonate concentration and the urine minus blood PCO2 difference in alkaline urine (U-B PCO2) and hence shed light on factors that influence hydrogen ion secretion in the collecting duct in vivo. The U-B PCO2 was used to monitor this latter parameter. In dogs with a normal extracellular fluid (ECF) volume, the U-B PCO2 was not primarily influenced by the urine bicarbonate concentration but rather it was related to the rate of sodium excretion. The U-B PCO2 could be abolished by amiloride when the urine bicarbonate concentration was less than 60 mm. At higher urine bicarbonate concentrations, there was a linear correlation between the U-B PCO2 and the urine bicarbonate concentration in normovolemic dogs given amiloride, but the absolute values were lower than they were in normovolemic animals not treated with amiloride. In the dogs with an expanded ECF volume, the U-B PCO2 was lower than it was in the normovolemic animals, and the U-B PCO2 was nor directly related to the urine bicarbonate concentration and not influenced by the rate of sodium excretion. Amiloride had little influence on the U-B PCO2 under these conditions. These results are interpreted to suggest that the magnitude of collecting duct hydrogen ion secretion is determined primarily by the electrical gradient generated by sodium reabsorption in normovolemic dogs and by the intracellular and lumenal hydrogen ion concentrations when the ECF volume is expanded or when active sodium reabsorption is inhibited by amiloride.

Absorption↗
PubMed1981

Effect of mineralocorticoids on collecting duct hydrogen ion secretion in the rabbit.

The purpose of this study was to elucidate the mechanism whereby a potassium infusion led to an elevation in the urine minus blood (ohm-B) PCO2 difference in alkaline urine of the rabbit. Rabbits given 9alpha-fluorohydrocortisone 16 h prior to study had a significantly high olm-B PCO2 than control rabbits. However, the ohm-B PCO2 was increased further after potassium infusion. These results suggest that the increased collecting duct hydrogen ion secretion in the rabbit may in part have been induced by mineralocorticoids and in addition been influenced by increasing the potassium concentration.

Acid-Base Equilibrium↗
PubMed1981

Implications of the finding of calcium carbonate in rabbit urine with respect to renal acidification.

Formation of calcium carbonate or carbamino compounds in a bicarbonate solution should generate hydrogen ions and thereby elevate the PCO2 of that solution. The presence of these substances in rabbit urine was established by demonstrating a significantly lower value for urine total carbon dioxide content measured by microgasometry (number of moles) than with the titration technique (number of equivalents). As there was a significant correlation between the calcium and the carbonate contents in the urine, we surmised that most of the carbonate was in the form of a suspension of calcium carbonate. Direct analysis of precipitates from rabbit bladders confirmed this impression. The formation of calcium carbonate in a solution should raise the PCO2 by the reaction: Ca2+ + 2HCO3- leads to CaCO3 + H2CO3 with subsequent dehydration of the H2CO3. In vitro studies demonstrated that the addition of 1 mmol calcium to 1 L of a 200 mM bicarbonate solution raised the PCO2 by approximately 50 mmHg (1 mmHg = 133.322 Pa). However, in vivo measurements of the PCO2 of rabbit urine containing a similar quantity of calcium carbonate revealed that there was no such rise in vivo (urine values = blood values). Therefore, the formation of calcium carbonate should have occurred at an earlier site in the nephron, thereby allowing the PCO2 to diffuse into peritubular capillaries during transit through the nephron.

Anaerobiosis↗
PubMed1980

Effect of blood pH on distal nephron hydrogen ion secretion.

The purpose o this study was to determine the effect of changes in blood hydrogen ion concentrations on urine acidification. The urine minus the blood PCO2 gradient in alkaline urine was used to monitor distal nephron hydrogen ion secretion. To obtain alkaline urine during acidemia, we induced proximal renal tubular acidosis by lysine. The urine minus the blood PCO2 gradient was evaluated relative to the urine bicarbonate concentration over a range of blood pH values. For any given urine bicarbonate concentration, the urine minus the blood PCO2 gradient was directly related to the blood hydrogen ion concentration. Conclusions. Acidemia stimulates and alkalemia inhibits distal nephron hydrogen ion secretion. Because the slope relating the urine minus the blood PCO2 gradient to the urine bicarbonate concentration was much steeper in urine from acidemic dogs, this change in relationship cannot be explained by a simple chemical equilibrium of the bicarbonate buffer system.

Acid-Base Equilibrium↗
PubMed1979

Irreversible renal failure following vesicoureteral reflux.

Antireflux surgery was performed in five patients with vesicoureteral reflux at a time when renal insufficiency was present. Notable proteinuria was present in four of the patients, and a kidney biopsy specimen showed glomerular lesions in one. Despite the eradication of reflux and of infection, all five patients continued to have progressive renal insufficiency culminating in renal failure. Vesicoureteral reflux nephropathy may include a glomerulopathy leading to progressive glomerular sclerosis. Antireflux surgery would not alter this ongoing process and therefore would not halt progressive renal failure.

Adult↗
PubMed1979

Influence of diet and metabolism on urinary acid excretion in the rat and the rabbit.

Rabbits normally excrete an alkaline urine, whereas rat urine is usually acidic. This study was designed to determine whether this difference was attributable to the composition of the diet or to specific metabolism of the species. Balance studies were performed in rabbits and rats with comparable growth rates who were consuming standard laboratory feed. The diets for both species had an excess of fixed cations over anions. Rats fed Rat Chow excreted urine containing net acid, whereas rabbits fed the same diet excreted urine containing net base. Rabbits eating Rabbit Chow excreted a very alkaline urine, but rats eating the same diet excreted much less alkali when expressed per kilogram of body weight. Balance studies demonstrated that rabbits absorbed a much higher proportion of dietary organic anions and excreted a larger fraction of this as total CO2. Collecting-duct hydrogen ion secretion and ammonium excretion, which are normally low in the rabbit during metabolic acidosis, were not increased when Rat Chow was consumed by rabbits for 2 weeks. In summary, feeding identical diets to rabbits or rats led to vastly different values for NAE. There appeared to be a gastrointestinal difference, as judged by the quantity of absorbed organic anions, as well as a metabolic difference reflected in the very different ratios of urinary total CO2 to organic anion.

Acid-Base Equilibrium↗