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Biomedical subjects

M B Goldstein

Publications and source records attributed to M B Goldstein.

At least 55 records · Page 3Linked to original sources
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

Studies on the mechanism whereby acidemia stimulates collecting duct hydrogen ion secretion in vivo.

The purpose of these studies was to elucidate the mechanism whereby collecting duct hydrogen ion secretion was augmented by acidemia. The urine minus blood PCO2 difference in alkaline urine (U-B PCO2) was used to evaluate this parameter. In dogs with a normal ECF volume, the U-B PCO2 factored was high, and there was no significant relationship between the U-B PCO2 factored for the urine bicarbonate concentration and the blood hydrogen ion concentrations unless amiloride, an agent that abolishes the transtubular potential difference, was present. In this latter case, the U-B PCO2 was a linear function of the urine bicarbonate concentration, and the U-B PCO2 factored for the urine bicarbonate concentration was directly proportional to the blood hydrogen ion concentration. To extend the pH range considerably, we used lysine to induce bicarbonaturia in dogs with an expanded ECF volume. Amiloride now caused only a small decrease in the U-B PCO2 at any urine bicarbonate concentration, and furthermore, it did not influence the linear relationship between the U-B PCO2 factored for the urine bicarbonate concentration and the blood hydrogen ion concentration. These results suggests that acidemia stimulates collecting duct hydrogen ion secretion by a mechanism that appears to be independent of the amiloride-sensitive component of the U-B PCO2. We speculate that the mechanism might involve an increased intracellular hydrogen ion concentration during acidemia.

Amiloride↗
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↗
PubMed1981

Selected aspects of the pathophysiology of metabolic acidosis in diabetes mellitus.

Metabolic acidosis with a normal anion gap results from either bicarbonate loss or a urine acidification defect. The bicarbonate loss may be via the gastrointestinal tract or the urine, or may be indirect due to excretion of the sodium and potassium as opposed to the ammonium salts of ketone body anions. Defects in urine acidification in the diabetic have several etiologies: first, hydrogen ion secretion may be decreased because of an intrinsic defect in the hydrogen ion pump (i.e., diseases of the renal medulla); second, there may be a failure to augment hydrogen ion secretion by a favorable electrical gradient (e.g., reduced mineralocorticoids); and third, there may be a failure to generate a favorable chemical gradient to augment hydrogen ion secretion (e.g., reduced urine ammonia). Reduced levels of aldosterone associated with hyporeninemia has been termed type IV RTA, and these patients have specific therapeutic needs.

Anions↗
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↗
PubMed1980

Renal biopsy in acute allograft rejection. Significance of moderate vascular lesions in long-term graft survival.

55 renal allograft biopsies obtained during acute rejection episodes resistant to standard antirejection therapy in 36 renal transplant recipients were reviewed and the findings correlated with long-term graft prognosis. 20 patients demonstrated moderate vascular pathology (group A), while 16 patients demonstrated changes consistent with pure cell-mediated rejection wit no vascular lesions (group B). Groups were similar with respect to age range, duration of haemodialysis, sex and antigen match. Of patients with vascular changes, 11 had arterial changes, 9 had arteriolar changes and 6 had arterial and arteriolar changes. The cumulative graft survival for group A was significantly less than that for group B at all post-transplantation intervals up to 24 months (p < 0.001).

Adult↗
PubMed1980

Interpersonal support and coping among first-year dental students.

Previous studies have suggested that individuals involved in supportive interpersonal relationships are buffered against the deleterious effects of stress. This hypothesis was evaluated in a dental school setting by examining the support networks of 63 first-year students. Levels of support were correlated with academic performance and indices of physical and psychological well-being. For men, social support was generally associated with better performance and well-being. Women, on the other hand, exhibited predominately negative relationships between support and all outcome measures. An unexpected finding for both men and women was the consistent, positive relationship between support and reported drug use. Tentative interpretations of the drug use findings as well as the paradoxical support-performance correlations for women are made. Several strategies for enhancing support system benefits are suggested.

Educational Measurement↗
PubMed1979

Pathogenesis of acidosis in hereditary fructose intolerance.

An 18-yr-old man with a classical history of hereditary fructose intolerance (HFI) developed typical biochemical changes following an oral fructose load: fructosemia, hypoglycemia, hypophosphatemia, hyperuricemia, and metabolic acidosis. Hypokalemia (3.1 meq/liter) was also noted. Three aspects of this case expand the published literature on this syndrome: (1) Metabolic acidosis was found to be due to both lactic acidosis and proximal renal tubular acidosis (RTA). We could quantitate the relative contribution of each, and found that urinary bicarbonate loss due to proximal RTA accounted for less than 10% of the fall in serum bicarbonate. The major cause of the metabolic acidosis was lactic acidosis. (2) Hypokalemia was found to be due to movement of potassium out of the extracellular space rather than to urinary loss. Potassium may have entered cells with phosphate or may have been sequestered in the gastrointestinal tract. (3) The coexistence of proximal RTA and acidemia made it possible to study the effect of acidemia on the urine-blood partial pressure of carbon dioxide (PCO2) gradient in alkaline urine (U-B PCO2). The U-B PCO2 measured during acidemia was much higher at the same urine bicarbonate concentration than in normal controls during alkalemia, providing evidence in humans that acidemia stimulates distal nephron hydrogen-ion secretion.

Acid-Base Imbalance↗
PubMed1979

Sources of stress and interpersonal support among first-year dental students.

Sixty-three first-year dental students were surveyed to gather information regarding sources of stress within the dental school environment and sources of interpersonal support. The results indicated that, as a group, dental students feel most stressed in regard to demands on their time, mastery of the volume of material presented, and inconsistent feedback from faculty. Significant sex differences emerged, with women reporting more stress associated with peer competition, fear of failure, fear of falling behind, and lack of positive feedback. Analysis of interpersonal support data revealed that women reported fewer peers as part of their support networks, especially in regard to task-oriented interactions. Possible strategies for reducing environmental stress and the development of support services for female students are considered in light of the findings.

Fear↗
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↗
PubMed1978

Disequilibrium pH and bicarbonate reabsorption: relevance to the pathogenesis of distal renal tubular acidosis.

An augmented renal capacity to reabsorb bicarbonate (RHCO3) has been noted in patients with distal renal tubular acidosis (dRTA), and construed as evidence that the basic defect in dRTA is abnormal distal tubular permeability. According to this interpretation, the absence of a disequilibrium pH due to a back-leak of H2C03 permits increased distal H+ secretion and results in an increased RHCO3. To test this assumption, we have evaluated the effect of acute elimination of the disequilibrium pH by carbonic anhydrase infusion. The results establish that this maneuver doses not cause a rise in RHCO3. Thus, the elevated value of RHC3 described in dRTA cannot be the consequence of increased back-diffusion of H2CO3 and is more likely due to coexisting extracellular volume depletion and/or postassium deficiency.

Acidosis, Renal Tubular↗