scholarly journals Idiopathic hypercalciuria: the contribution of Dr. Jacob Lemann, Jr.

1994 ◽  
Vol 5 (5) ◽  
pp. S59
Author(s):  
F L Coe ◽  
J H Parks
Keyword(s):  
Mineral Metabolism ◽  
Idiopathic Hypercalciuria ◽  
Acid Base Balance ◽  
Acid Base ◽  
Carbohydrate Ingestion ◽  
Low Calcium Diet ◽  
Base Balance ◽  
Acid Base Status ◽  
Normal Men ◽  
Calcium Loss

The original contributions of Jacob Lemann to mineral metabolism, especially calcium metabolism and idopathic hypercalciuria, are reviewed. One group of studies concern acid base balance and calcium loss, showing that acid loads increase calcium loss in the urine. Another group of studies concern the calciuria of glucose or carbohydrate ingestion, with the observation that stone patients, who as a population are enriched with hypercalciuria, respond with more exaggerated calciuria to glucose loads than do normal people. Yet another body of work shows that normal men, when given noncalcemic loads of calcitriol, exhibit two essential features of idiopathic hypercalciuria--hyperabsorptive hypercalciuria and bone mineral loss on a low-calcium diet. The final group of studies presented worked on the problem of thiazide hypocalciuric action, and where the calcium goes that does not appear in the urine, as well as the effects of potassium bicarbonate and sodium loads on mineral balance and acid base status.

scholarly journals Effect of anionic salts on some blood and urine minerals, acid-base balance and udder oedema of dry pregnant cows

2003 ◽  
Vol 12 (2) ◽  
pp. 83-93 ◽  
Author(s):  
S. TAURIAINEN ◽  
S. SANKARI ◽  
S. PYÖRÄLÄ
Keyword(s):  
Mineral Metabolism ◽  
Acid Base Balance ◽  
Dry Period ◽  
Acid Base ◽  
Grass Silage ◽  
Base Balance ◽  
Concentrate Mixture ◽  
Blood And Urine Samples ◽  
Acid Base Status ◽  
Friesian Cows

The objective of this study was to determine the effect of an anionic diet on mineral metabolism, acid-base status and udder oedema of dairy cows fed grass silage based diets during the dry period. Eighteen pregnant, non-lactating Friesian cows were divided randomly into two groups according to their expected calving date. Dietary cation-anion balance (DCAB), calculated as mill equivalents [(Na + + K + ) - (Cl - + S 2- )], for high DCAB (control) and low DCAB treatments were +254 and -41 mEq kg -1 dry matter (DM), respectively. Anionic salts were ammonium chloride (NH 4 Cl), magnesium chloride (MgCl 2 ) and magnesium sulphate (MgSO 4 ). Cows received grass silage (5.2 kg DM), hay (0.9 kg DM) and a concentrate mixture (2.7 kg DM) until calving. Blood and urine samples were collected 4, 3, 2 and 1 week before the expected calving date, at calving, 1 day and 1 week after calving. Udder oedema was evaluated by a quantitative and a subjective method. Acidification resulted in a marked decrease in urinary pH, increased urinary Ca excretion and a change in blood acidbase balance. Blood Ca 2+ and plasma Ca tot concentrations were more stable at parturition for the anionic group, although such differences were not statistically significant. Anionic salts (DCAB -41 mEq kg -1 DM) did not cause udder oedema in experimental cows.;

Prepartum level of dietary cation-anion difference fed to nulliparous cows: Acid-base balance, mineral metabolism, and health responses

2021 ◽  
Author(s):  
R. Zimpel ◽  
M. Nehme Marinho ◽  
K.V. Almeida ◽  
A. Revilla Ruiz ◽  
M.C. Perdomo ◽  
...  
Keyword(s):  
Mineral Metabolism ◽  
Acid Base Balance ◽  
Acid Base ◽  
Base Balance

Relationship between acid-base balance and the central respiratory mechanisms

1963 ◽  
Vol 204 (5) ◽  
pp. 867-872 ◽  
Author(s):  
R. L. Katz ◽  
S. H. Ngai ◽  
G. G. Nahas ◽  
S. C. Wang
Keyword(s):  
Periodic Breathing ◽  
Acid Base Balance ◽  
Acid Base ◽  
Respiratory Effects ◽  
Inspiratory Phase ◽  
Arterial Ph ◽  
Base Balance ◽  
Acid Base Status ◽  
Definition Of ◽  
Functional Components

To study the effect of changes in acid-base balance on respiratory patterns, 2-amino-2-hydroxymethyl-1,3-propanediol (THAM, an organic buffer) and sodium bicarbonate (NaHCO3) were infused into midcollicular decerebrate, pontile, and medullary cats. NaHCO3 increased the arterial pH, HCO–3, and pCO2. THAM increased the arterial pH and HCO–3. The arterial pCO2 fell initially and then rose gradually with time. In the midcollicular decerebrate preparation with eupnea, NaHCO3 increased while THAM decreased the rate and amplitude of respiration. In the vagotomized pontile preparation with apneustic breathing, NaHCO3 accelerated and THAM decelerated the apneustic cycling; neither produced a significant change in amplitude. Larger doses of THAM abolished the apneustic cycling either by producing expiratory apnea or by prolonging the inspiratory phase. In the medullary preparation with periodic breathing, THAM decreased the rate with minimal changes in amplitude. The findings suggest that the respiratory effects of NaHCO3 and THAM were due to changes in intracellular pH and pCO2 and that all functional components of the respiratory center are influenced by changes in the acid-base status of the animals. Finally it is pointed out that elucidation of neural respiratory mechanisms requires definition of the acid-base state of the animal.

Gastric mucosal repair and release of HCO3- after damage by 2 M NaCl in cat: role of systemic acid base status

1994 ◽  
Vol 267 (4) ◽  
pp. G536-G545 ◽  
Author(s):  
K. Guttu ◽  
K. Grong ◽  
K. Svanes ◽  
J. E. Gronbech
Keyword(s):  
Mucosal Blood Flow ◽  
Mucosal Damage ◽  
Major Influence ◽  
Acid Base Balance ◽  
Acid Base ◽  
Mucosal Repair ◽  
Base Balance ◽  
Acid Base Status ◽  
Hyperemic Response

To study the influence of acid base balance on gastric mucosal repair, NH4Cl or NaHCO3 was given intravenously to anesthetized cats after mucosal damage induced by intraluminal 2 M NaCl. Saline at pH 5 or 1 was perfused via an oral tube through the stomach lumen and evacuated via a pyloric tube to a chamber with pH and PCO2 electrodes. Luminal bicarbonate (HCO3-) was markedly increased early after damage in both acidotic and alkalotic animals. In alkalotic animals mucosal blood flow increased about twofold in response to mucosal damage, whereas the early hyperemic response was either completely attenuated or blunted in acidotic animals. HCO3- release was correlated to availability of HCO3- by blood in alkalotic animals with luminal pH 5. Alkalotic animals showed improved repair compared with acidotic animals, and mucosal restitution was correlated to availability of HCO3- by blood. We conclude that luminal leakage of HCO3- or plasma after mucosal damage depends on availability by blood and consumption of HCO3- within the mucosa and that blood borne HCO3- has a major influence on gastric mucosal repair.

Role of iNOS and eNOS in modulating proximal tubule transport and acid-base balance

2002 ◽  
Vol 283 (4) ◽  
pp. F658-F662 ◽  
Author(s):  
Tong Wang
Keyword(s):  
Proximal Tubule ◽  
Knockout Mice ◽  
Proximal Tubules ◽  
Wild Type ◽  
Acid Base Balance ◽  
Acid Base ◽  
Base Balance ◽  
Acid Base Status ◽  
Inos Knockout Mice ◽  
Oxide Synthase

Our laboratory has previously shown that mice lacking neuronal nitric oxide synthase (nNOS) are defective in fluid absorption ( J v) and HCO[Formula: see text]absorption ( J HCO3) in the proximal tubule and develop metabolic acidosis. The present study examined the transport of fluid and HCO[Formula: see text] in the proximal tubule and acid-base status in mice lacking two other isoforms of NOS, inducible NOS (iNOS) and endothelial NOS (eNOS). Proximal tubules were microperfused in situ in wild-type and NOS knockout mice by methods previously described (Wang T, Yang C-L, Abbiati T, Schultheis PJ, Shull GE, Giebisch G, and Aronson PS. Am J Physiol Renal Physiol 277: F298–F302, 1999). [3H]inulin and total CO2 concentrations were measured in the perfusate and collected fluid, and net J v and J HCO3 were analyzed. These data show that J HCO3 was 35% lower (71.7 ± 6.4 vs. 109.9 ± 7.3 pmol · min−1 · mm−1, n = 13, P < 0.01) and J v was 38% lower (0.95 ± 0.15 vs. 1.54 ± 0.17 nl · min−1 · mm−1, n = 13, P < 0.05) in iNOS knockout mice compared with their wild-type controls. Addition of the iNOS-selective inhibitor l- N 6-(1-iminoethyl) lysine, reduced both J v and J HCO3 significantly in wild-type, but not in iNOS knockout, mice. In contrast, both J HCO3(93.3 ± 7.9 vs. 110.6 ± 6.18 pmol · min−1 · mm−1) and J v (1.56 ± 0.17 vs. 1.55 ± 0.16 nl · min−1 · mm−1) did not change significantly in eNOS knockout mice. These results indicated that iNOS upregulates Na+ and HCO[Formula: see text]transport, whereas eNOS does not directly modulate Na+ and HCO[Formula: see text] transport in the kidney proximal tubules.

Evaluation of bicarbonate transport in rat distal tubule: effects of acid-base status

1982 ◽  
Vol 243 (4) ◽  
pp. F335-F341 ◽  
Author(s):  
M. S. Lucci ◽  
L. R. Pucacco ◽  
N. W. Carter ◽  
T. D. DuBose
Keyword(s):  
Metabolic Acidosis ◽  
Respiratory Acidosis ◽  
Distal Tubule ◽  
Bicarbonate Transport ◽  
Acid Base Balance ◽  
Acid Base ◽  
Bicarbonate Reabsorption ◽  
Base Balance ◽  
Acid Base Status ◽  
Acute Metabolic Acidosis

Previous micropuncture studies utilizing indirect methods to estimate bicarbonate transport in the rat superficial distal tubule have indicated that the distal bicarbonate reabsorptive process normally operates well below the saturation level. Recent studies from our laboratory failed to demonstrate a spontaneous acid disequilibrium pH in this segment, implying that the bicarbonate reabsorptive rate was less than previously estimated. The purpose of the present experiments were 1) to measure the rate of absolute bicarbonate reabsorption by the rat superficial distal tubule while controlling bicarbonate delivery, and 2) to examine the effects of alterations in acid-base status on the rate of bicarbonate reabsorption. Five groups of rats in different states of acid-base balance were studied. No significant bicarbonate reabsorption was detected in the control hydropenic, combined respiratory acidosis-metabolic alkalosis, acute respiratory acidosis, or acute metabolic acidosis groups. In contrast, metabolic acidosis of 3 days duration resulted in a significant bicarbonate reabsorptive rate of 52.6 +/- 13.9 pmol . mm-1 . min-1. The observation of significant bicarbonate reabsorption in the distal tubule only during chronic metabolic acidosis of 3 days duration is compatible with adaptation of this normally low-capacity segment to chronic changes in systemic acid-base states.

Glucose and lactate turnover and gluconeogenesis in chronic metabolic acidosis and alkalosis in normal and diabetic dogs

1988 ◽  
Vol 66 (1) ◽  
pp. 140-145 ◽  
Author(s):  
G. Hetenyi Jr. ◽  
H. Paradis ◽  
J. Kucharczyk
Keyword(s):  
Metabolic Acidosis ◽  
Plasma Glucose ◽  
Turnover Rate ◽  
Moderate Degree ◽  
Acid Base Balance ◽  
Acid Base ◽  
Lactate Turnover ◽  
Base Balance ◽  
Acid Base Status ◽  
Diabetic Dogs

The turnover rate of glucose, the irreversible disposal rate of lactate, and the rate of gluconeogenesis from lactate were calculated by tracer methods in four normal and four alloxan-diabetic dogs under control conditions as well as in chronic, stable metabolic acidosis and alkalosis. Acidosis was produced by feeding dogs 0.8–1 g∙kg−1∙day−1 NH4Clover 1 week, alkalosis was produced by feeding dogs a chloride-free diet and injections of furosemide. Mean plasma pH in the three states were 7.28 ± 0.013, 7.40 ± 0.024, and 7.51 ± 0.015 in normal dogs, and 7.22 ± 0.025,7.42 ± 0.009, and 7.49 ± 0.002 in the diabetic dogs. Respective mean plasma bicarbonate levels were 14.6 ± 0.88, 22.0 ± 0.80, and 32.4 ± 1.88 mequiv. in normal dogs, and 12.3 ± 1.30, 22.6 ± 0.66, and 35.0 ± 1.14 mequiv. in diabetic animals. In normal dogs shifts in acid–base balance had no effect on the level of plasma glucose or the turnover rate of glucose. In diabetic dogs plasma glucose level was significantly elevated by alkalosis. Plasma lactate was positively correlated with plasma pH(r = 0.69, p < 0.01) and was in general higher in diabetic than in normal animals. The increment in concentration was due to a decreased clearance of lactate from the plasma. The irreversible disposal rate was not changed by the acid–base status. Whereas a larger fraction of lactate removed from the plasma appeared in glucose in diabetic animals, this fraction was not changed significantly by shifts in the acid–base status. The glycemic response to i.v. injected 0.05 U/kg insulin was not appreciably altered by the shifts in acid–base status in either normal or diabetic dogs. Stable metabolic acidosis and alkalosis of moderate degree has little effect on glucose and lactate kinetics and gluconeogenesis from lactate in either normal or diabetic dogs.

Is urea formation regulated primarily by acid-base balance in vivo?

1986 ◽  
Vol 250 (4) ◽  
pp. F605-F612 ◽  
Author(s):  
M. L. Halperin ◽  
C. B. Chen ◽  
S. Cheema-Dhadli ◽  
M. L. West ◽  
R. L. Jungas
Keyword(s):  
Dietary Protein ◽  
Urea Synthesis ◽  
Acid Base Balance ◽  
Severe Metabolic Acidosis ◽  
Acid Base ◽  
Wide Range ◽  
Base Balance ◽  
Acid Load ◽  
Acid Base Status

Large quantities of ammonium and bicarbonate are produced each day from the metabolism of dietary protein. It has recently been proposed that urea synthesis is regulated by the need to remove this large load of bicarbonate. The purpose of these experiments was to test whether the primary function of ureagenesis in vivo is to remove ammonium or bicarbonate. The first series of rats were given a constant acid load as hydrochloric acid or ammonium chloride; individual rats received a constant nitrogen load at a time when their plasma acid-base status ranged from normal (pH 7.4, 28 mM HCO3) to severe metabolic acidosis (pH 6.9, 6 mM HCO3). Urea plus ammonium excretions and the blood urea, glutamine, and ammonium concentrations were monitored with time. Within the constraints of non-steady-state conditions, the rate of urea synthesis was constant and the plasma glutamine and ammonium concentrations also remained constant; thus it appears that the rate of urea synthesis was not primarily regulated by the acid-base status of the animal in vivo over a wide range of plasma ammonium concentrations. In quantitative terms, the vast bulk of the ammonium load was converted to urea over 80 min; only a small quantity of ammonium appeared as circulating glutamine or urinary ammonium. Urea synthesis was proportional to the nitrogen load. A second series of rats received sodium bicarbonate; urea synthesis was not augmented by a bicarbonate load. We conclude from these studies that the need to dispose of excess bicarbonate does not primarily determine the rate of ureagenesis in vivo. The data support the classical view that ureagenesis is controlled by the quantity of ammonium to be removed.

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