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PubMed1990

Metabolic characteristics of cat kidney: failure to adapt to metabolic acidosis.

During studies performed on domestic cats made acidotic with ammonium chloride, it was found that the cat kidney is unable to adapt to metabolic acidosis. Renal proximal tubules do not increase their production of ammonia or glucose from glutamine during acidosis. During in vivo studies, the renal excretion of ammonia did not change much during acidosis. Other metabolic parameters in the cat were not very different from those found in other animals such as rat or dog. However, it was found that cats may show a relatively high plasma glucose concentration compared with other animals. Plasma insulin concentration was normal, and the animals showed no evidence of diabetes mellitus. It is not known whether limitation of ammoniagenesis and elevated plasma glucose concentration also characterize larger felidae such as panthers and cougars.

Acid-Base Equilibrium↗
PubMed1994

Lactic acidosis transiently increases metabolic rate of turtle myocytes.

We measured O2 consumption as an estimate of metabolic rate in isolated calcium-tolerant ventricular myocytes of turtles (Chrysemys picta belli) at control pH 7.8 and in the same solution brought to pH 7.4 and 7.0 with additions of lactic acid. Our aim was to test the hypothesis that lactic acidosis caused metabolic depression by initiating downregulation of Na+ channels, and thus Na(+)-K(+)-ATPase (Na+ pump) activity, which we would measure as a decrease in O2 consumption. Myocyte O2 consumption was measured in reptilian N-tris(hydroxymethyl)methyl-2-aminoethanesulfonic acid-buffered Ringer solution and in nomially Na(+)- and Ca(2+)-free solution, thus estimating the Na+ pump component of metabolic rate. Lowering extracellular pH from 7.8 to 7.0 resulted in a significant increase in metabolic rate of cells in Ringer solution but not those in Na(+)- and Ca(2+)-free solution. This result was unchanged by the addition of 2 mM Ca2+ to Na(+)-free cell suspensions, indicating that the difference was due to the presence of Na+. Addition of 100 microM amiloride to cells in Ringer solution at pH 7.0 abolished the increase in O2 consumption, suggesting that the apparent increase in Na(+)-K(+)-ATPase activity was secondary to Na(+)-H+ exchange. Intracellular pH was measured using 5,5-dimethyl[14C]oxazolidine-2,4-dione. Cells treated with amiloride and those in Na(+)- and Ca(2+)-free solution did not regulate intracellular pH following acidosis and maintained basal metabolic rate. These data suggest that the Na(+)-H+ exchanger is an important contributor to intracellular pH regulation in the myocyte but increases Na+ pump activity and metabolic rate immediately following acidosis.

Acidosis, Lactic↗
PubMed1995

Effects of input pressure on in vitro turtle heart during anoxia and acidosis: a 31P-NMR study.

In vitro working hearts of the turtle, Chrysemys picta bellii, paced at 30 beats/min, were studied over a range of input pressures in the following sequence of perfusion conditions: control normoxia, control anoxia, lactacidotic normoxia, and lactacidotic anoxia. Two such series of experiments were performed. In series 1 (n = 12), ventricular pressure (PV) and cardiac output were measured, and power output and dPV/dt were calculated. In series 2 (n = 5), intracellular phosphorus metabolites and intracellular pH (pHi) were also measured using 31P-nuclear magnetic resonance (31P-NMR) spectroscopy. In series 1 all mechanical variables increased with input pressure in generally similar fashion, except during anoxic acidosis, during which mechanical performance was depressed and was increased less or not at all by input pressure. Creatine phosphate (CP) and pHi fell significantly in anoxia and anoxic acidosis, but neither these variables, ATP, CP/ATP, nor, presumably, ADP changed as a function of input pressure with any perfusate despite often large increments in mechanical output. We conclude that anoxia and acidosis act synergistically to depress cardiac function in turtle hearts. Also, the insensitivity of NMR variables to changes in input pressure and cardiodynamics suggests that changes in these variables are unimportant for controlling energy turnover in this preparation.

Acidosis↗
PubMed1983

Metabolic acidosis and parathyroidectomy increase Na+-H+ exchange in brush border vesicles.

Na+-H+ exchange across the brush border membrane of the renal proximal tubular cell is a mechanism for Na+ reabsorption and H+ secretion. An electroneutral Na+-H+ exchange activity has been identified in isolated renal brush border membrane vesicles from rat and dog kidney, and increased Na+-H+ exchange has been measured in brush border membrane vesicles from remnant kidneys of dogs with chronic renal failure. To ascertain whether changes in H+ secretion by the kidney observed in chronic metabolic acidosis and in states of altered parathyroid function might result from altered Na+-H+ exchange across the renal cortical cellular brush border membrane, we measured Na+-H+ exchange in brush border membrane vesicles from kidneys of dogs with chronic metabolic acidosis and from kidneys of thyroparathyroidectomized dogs. Increased amiloride-sensitive Na+-H+ exchange was demonstrated in brush border membrane vesicles from kidneys of both groups of dogs, suggesting that adaptations in H+ excretion in chronic metabolic acidosis and hypoparathyroidism might be explained by increased activity of a renal brush border membrane Na+-H+ exchanger.

Acidosis↗
PubMed1984

Increased Vmax for Na+/H+ antiporter activity in proximal tubule brush border vesicles from rabbits with metabolic acidosis.

Na+/H+ antiporter activity in renal brush border vesicles from control rabbits and rabbits made acidotic with 3 days of NH4Cl gavage was measured using the acridine orange method. Acidotic rabbits exhibited a significantly higher Vmax for antiporter activity (2.80 +/- 0.45 fluorescence units X s-1 X mg protein-1) compared with controls (1.31 +/- 0.13) but the Km for Na+ was unchanged (23.7 +/- 3.5 for acidotic, 19.1 +/- 3.2 mM for controls). When the Vmax for Na+/H+ antiporter activity was considered in relation to the degree of acidosis achieved in the experimental animals, there was a correlation (r = -0.75) between Vmax and plasma total CO2 concentration. Amiloride (100 microM) inhibited Na+/H+ exchange (Na+ = 90 mM) by 59 +/- 7% in both control and acidotic animals, indicating that the observed stimulation in Na+/H+ antiporter activity was not due to increased electrically coupled cation exchange. These findings suggest that the response of the proximal tubule to chronic metabolic acidosis involves an adaptive increase in the Vmax for Na+/H+ antiporter activity in the brush border membrane that is correlated to the degree of acidosis in the animals.

Acidosis↗
PubMed1984

Glutamine transport in basolateral vesicles from dogs with acute respiratory acidosis.

It has been shown that acute respiratory acidosis in dogs results in enhanced renal extraction of L-glutamine from plasma and increased ammonia excretion per nephron. To determine whether a component of the enhanced L-glutamine extraction results from increased transport of L-glutamine across the basolateral membrane into the renal proximal tubular cell, we measured Na+ gradient-dependent L-[3H]glutamine transport in proximal tubular basolateral membrane vesicles isolated from kidneys of normal dogs and from kidneys of dogs following 2 h of acute respiratory acidosis. The initial rate of Na+ gradient-dependent L-[3H] glutamine uptake (15 s) was increased significantly in basolateral membrane vesicles from the acidotic compared with normal dogs. Increased uptake could be measured under conditions in which changes in membrane potential resulting from fluxes of solute were minimized. We conclude that an adaptation occurs in the basolateral membrane of the renal proximal tubular cell during acute respiratory acidosis that allows increased transport of L-glutamine across the membrane into the proximal tubular cell. This adaptation may permit increased ammonia production per nephron.

Acid-Base Equilibrium↗
PubMed1985

Response of serum 1,25(OH)2D3 to variation of ionized calcium during chronic acidosis.

Chronic ammonium chloride (NH4Cl) administration causes metabolic acidosis and prevents the normal rise of serum 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] during a low-calcium diet (LCD, 0.002% calcium). The suppression of serum 1,25(OH)2D3 was not due to reduced parathyroid hormone concentration, elevated serum phosphorus, or total calcium concentration. Acidosis increased blood ionized Ca [Ca2+] and proton [H+] concentrations. Serum 1,25(OH)2D3 levels were inversely correlated with both [Ca2+] and [H+]. To determine the independent effects of [Ca2+] on serum 1,25(OH)2D3 we varied [Ca2+] at a constant [H+] by infusing either EGTA or saline for 24 h after 11 days of LCD and NH4Cl. EGTA, preequilibrated with three concentrations of Ca, lowered [Ca2+] and raised 1,25(OH)2D3 but did not alter [H+] or serum phosphorus concentration. The log of serum 1,25(OH)2D3 varied linearly and inversely with arterial blood [Ca2+] during saline (r = -0.884, n = 8, P less than 0.001) and EGTA infusions (r = -0.798, n = 22, P less than 0.001). At all levels of [Ca2+], rats infused with EGTA had a higher serum 1,25(OH)2D3 than those infused with saline. Log serum 1,25(OH)2D3 was correlated neither with [H+] nor pH. Elevated [Ca2+] and not [H+] appears to suppress the serum 1,25(OH)2D3 response to LCD during NH4Cl acidosis in the rat.

Acidosis↗
PubMed1985

Metabolic effects of sodium bicarbonate in hypoxic lactic acidosis in dogs.

The metabolic effects of NaHCO3 therapy in hypoxic lactic acidosis were evaluated in the anesthetized dog. Hypoxic lactic acidosis was induced by ventilating the dogs with a hypoxic gas mixture of 8% O2/92%N2, resulting in arterial PO2 of less than 30 mmHg, pH below 7.20, bicarbonate less than 12 mM, and lactate more than 7 mM. In this situation lactate accumulates because of overproduction of lactate by gut and carcass in the presence of a diminished capacity of the liver to extract lactate. After the development of hypoxic lactic acidosis the dogs were treated for 60 min with either NaHCO3 or NaCl or had no therapy. Sixty minutes of either treatment resulted in further declines of blood pH and bicarbonate that were similar in all three groups. NaHCO3-treated animals, however, showed an increase in blood lactate that were significantly higher than those treated with NaCl or those that had no therapy. This could be explained by a significantly higher gut lactate production with NaHCO3 therapy than in the NaCl-treated group. Concomitantly NaHCO3-treated animals showed a decrement in liver and gut blood flow that did not occur with NaCl treatment. Only NaHCO3 therapy was associated with a further decrease of liver intracellular pH, which could be attributed to both an increase in the CO2 load to the liver and increased tissue lactate levels, which were not observed with NaCl or no therapy. Additionally, liver lactate extraction was not improved by administration of NaHCO3 or NaCl.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗
PubMed1987

Interorgan glutamine flow in metabolic acidosis.

Acid-base homeostasis depends on glutamine flow from producer organs to those capable of generating bicarbonate. Glutamine oxidation, the prerequisite metabolic transformation, can be expressed by many sites; however, net base generation requires that glutamine flow be directed to a specific organ, the kidney. Normally, glutamine flows from the periphery to the splanchnic bed, providing a major fuel and supporting ureagenesis. Glutamine flow in chronic metabolic acidosis, on the other hand, is rerouted to the kidneys; asymmetrical distribution of NH+4 and HCO3- into the urine and renal vein subserves restoration of alkaline reserves. Clearly, glutamine flows in accordance with physiological demands, yet little is known of the regulatory mechanisms. As a model, chronic metabolic acidosis alters two aspects of this vital flow, its direction and magnitude. Characteristically the direction of flow is away from the splanchnic bed and into the kidneys associated with a marked fall in arterial glutamine concentration, restoring arterial level returns flow to the splanchnic bed sink. Thus glutamine homeostasis is sacrificed to impart direction to interorgan glutamine flow. Although multiple sites contribute to glutamine homeostasis, of great strategic importance is the potent hepatic glutaminase flux activated by portal venous NH+4 fed forward by gut metabolism; local hydrogen ion concentration modulates the effectiveness of this activator. Acute regulation of flow direction can be exerted by the lungs in determining the prevailing pCO2 and cellular acidity; respiratory compensation in chronic acidosis allows the expression of hepatic glutaminase, thereby suppressing arterial glutamine concentration. The enormous magnitude of glutamine flowing from muscle to the kidneys is supported by adaptive increases in glutamine synthetase and mitochondrial glutaminase, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1988

Renal adaptation to metabolic acidosis in senescent rats.

In this study, we compared results obtained in senescent rats with young rats given an equivalent acid load. We examined the renal changes by giving equivalent acid loads for 48 h to both 6- and 24-mo-old rats. The basal excretion of ammonium was the same in both groups, whereas titratable acids, phosphate, and Ca2+ excretions were increased in the senescent animal. After administration of the acid load, ammonium, phosphate, Ca2+, and titratable acid excretions increased in both age groups, but there were greater absolute increases in ammonium and titratable acid excretions in the young rats. The total acid excreted by the 24-mo rats was reduced 50 (day 1) and 25% (day 2) compared with the young rats, which was reflected by the more severe acidosis in those animals. The portion of total acid excreted as titratable acids in senescent animals was also increased during acidosis when compared with the young animals. In isolated proximal tubule brush-border membrane vesicles, acidosis increased Na+-H+ exchange and decreased Na+-dependent phosphate transport in both age groups. We also found that the basal activity of the Na+-H+ exchanger was not changed with age but the Na+-dependent phosphate transporter was less in the 24-mo rat. The results suggest that physiological regulation of these renal processes remains intact in the aged rat but the responses may be reduced or delayed in the senescent animal.

Acclimatization↗
PubMed1989

Effect of acute metabolic acidosis on ammonia metabolism in kidney.

To understand the mechanisms that initiate the increase in ammonia formation during acute acidosis in kidney [amino-15N]- and [amino-15N]glutamine were used as substrates in isolated perfused rat kidney experiments. Perfused kidneys from methionine sulfoximine-treated rats take up glutamine nitrogen at the rate of 1.50 +/- 0.08 mumol.g kidney-1.min-1 while forming ammonia at a rate of 0.65 +/- 0.09 mumol.g.kidney-1.min-1. Mass spectrometer analysis of the perfusate and urine reveals that ammonia is formed from the amide nitrogen of glutamine at the rate of 0.32 +/- 0.06 mumol.g kidney-1.min-1 and ammonia is formed from glutamate derived from glutamine at the rate of 0.21 +/- 0.04 mumol.g kidney-1.min-1. The balance of the ammonia formed is from unidentified endogenous sources. Addition of HCl to the perfusate to lower perfusate pH increases ammonia formation to 1.09 +/- 0.10 mumol.g kidney-1.min-1. The results exclude a role for the purine nucleotide cycle during acute acidosis and confirm that ammonia formation from glutamate derived from glutamine is via glutamate dehydrogenase. Lowering perfusate pH increases the rate of glutamine deamidation significantly by 0.33 +/- 0.06 mumol.g kidney-1.min-1 and increases the rate of ammonia formation via glutamate dehydrogenase insignificantly by only 0.08 +/- 0.04 mumol.g kidney-1.min-1, whereas ammonia formation from endogenous sources remains unchanged. The results demonstrate that regulation of glutamine deamidation is an important controlling step in ammonia formation during acute metabolic acidosis in kidney.

Acidosis↗
PubMed1994

Extracellular acidosis minimizes actin cytoskeletal alterations during ATP depletion.

Extracellular acidosis has been shown to be protective during ischemia in renal tubule cells. However, the mechanism of protection remains unknown. Since ischemia leads to disruption and polymerization of the cortical actin cytoskeleton, we hypothesized acidosis may better preserve the actin cytoskeleton during ischemia. Therefore, the purpose of our studies was to examine the effect of pH on the integrity of the actin cytoskeleton during ATP depletion and ATP repletion. To do this, we used an in vitro model of reversible ATP depletion in LLC-PK1 cells at extracellular pH values (pHo) of 6.9, 7.4, and 7.9. Immunofluorescent studies with rhodamine-phalloidin demonstrated more marked redistribution and clumping of cortical actin at pHo 7.9 and 7.4 vs. 6.9 after 90 min of chemical anoxia. After 15 min of ATP depletion, G-actin, quantified by the deoxyribonuclease assay, decreased from 53.7 +/- 0.8 to 43.2 +/- 1.5 microgram/mg protein at pHo 6.9 vs. 37.6 +/- 1.8 microgram/mg protein at pHo 7.4 (P < 0.001). After 60 min, there still was significantly less conversion of G-actin to F-actin at pHo 6.9 vs. 7.4, with a decrease from 55.9 +/- 2.0 to 39.6 +/- 2.0 micrograms/mg protein at 6.9 vs. 35.8 +/- 2.4 at 7.4 micrograms/mg protein (P < 0.05). Furthermore, extracellular acidosis during the phase of ATP repletion resulted in more rapid normalization of cellular G-actin levels (95 +/- 3% of control vs. 82 +/- 2% for pH 6.9 vs. 7.4, respectively, P < 0.01). Together, these findings indicate the actin cytoskeleton is better preserved in an acidic environment during ATP depletion.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗
PubMed1998

Carbonic anhydrase II and IV mRNA in rabbit nephron segments: stimulation during metabolic acidosis.

Carbonic anhydrase (CA) facilitates renal bicarbonate reabsorption and acid excretion. Cytosolic CA II catalyzes the buffering of intracellular hydroxyl ions by CO2, whereas membrane-bound CA IV catalyzes the dehydration of carbonic acid generated from the secretion of protons. Although CA II and IV are expressed in rabbit kidney, it is not entirely clear which segments express which isoforms. It was the purpose of this study to characterize the expression of CA II and CA IV mRNAs by specific segments of the nephron using semiquantitative reverse transcription-polymerase chain reaction (RT-PCR) and to determine the effect of chronic metabolic acidosis on CA expression by those segments. Individual nephron segments (usually 1-2 mm) were isolated by microdissection and subjected to RT-PCR. Amplification was performed simultaneously for CA IV, CA II, and malate dehydrogenase (MDH), a housekeeping gene. The intensities of the PCR products were quantitated by densitometry. CA IV mRNA was expressed by S1 and S2 proximal tubules and by outer medullary collecting duct from inner stripe (OMCDi) and outer stripe and initial inner medullary collecting duct (IMCDi). CA II mRNA was expressed by S1, S2, and S3 proximal tubules, thin descending limb, connecting segment (CNT), and all collecting duct segments. Acid loading induced CA IV mRNA expression in S1 and S2 proximal tubules and in OMCDi and IMCDi. CA II mRNA was induced by acidosis in all three proximal segments and nearly all distal segments beginning with CNT. No upregulation of MDH mRNA expression occurred. These adaptive increases in CA II and IV mRNAs are potentially important in the kidney's adaptation to chronic metabolic acidosis.

Acidosis↗
PubMed1983

Changes in brain ECF pH during metabolic acidosis and alkalosis: a microelectrode study.

We used pH-sensitive double-barreled microelectrodes to measure brain extracellular fluid (ECF) pH in anesthetized dogs during isocapnic infusion acidosis (HCl) and alkalosis (Na2CO3) of 45-60 min duration. The diameter of the tips of these electrodes varied from less than 1 to 27 micron and were placed 5 mm below the surface of the parietal cortex. In group I (metabolic acidosis, n = 5) mean plasma and brain ECF pH fell significantly by 0.221 and 0.025, respectively, with changes in brain ECF pH being 11.3% of those noted in plasma. In group II (metabolic alkalosis, n = 5) mean plasma and brain ECF pH rose significantly by 0.170 and 0.049, respectively, with changes in brain ECF pH being 28.8% of those noted in plasma. Mean arterial and sagittal venous PCO2 and cisternal cerebrospinal fluid (CSF) acid-base variables did not change significantly during acid or base infusion. We conclude that during transients of isocapnic metabolic acid-base perturbations ionic gradients exist between brain ECF and CSF and that changes in brain ECF pH measured by microelectrodes follow the changes in plasma pH. These pH changes may play an important role in respiratory adaptations of acute metabolic acidosis and alkalosis.

Acidosis↗
PubMed1992

Group B Streptococcus-induced acidosis in newborn swine: regional oxygen transport and lactate flux.

To investigate the mechanism of metabolic acidosis resulting from group B streptococcal sepsis, oxygen metabolism and lactate flux of the cerebrum, hindlimb, liver, splanchnic organs, and systemic vascular bed as a whole were examined. Nine 3- to 5-day-old awake and spontaneously breathing piglets were studied before and after 3, 4, and 5 h of continuous live group B Streptococcus infusion. After 5 h, oxygen delivery was decreased to all organs and to the whole systemic vascular bed. Increased oxygen extraction compensated for reduced oxygen delivery in the liver and splanchnic organs; however, it only partially offset reduced oxygen delivery to the hindlimb and systemic vascular bed. Cerebral oxygen extraction did not increase. As a result, oxygen uptake was reduced in the cerebrum, hindlimb, and systemic vascular bed. At 5 h of bacterial infusion, arterial lactate concentration was increased with regional lactate efflux from the cerebrum and hindlimb and influx to the liver (P less than 0.05 vs. zero or no net flux). We conclude that group B Streptococcus-induced metabolic acidosis is associated with regional lactate efflux from vascular beds in which oxygen uptake is reduced. We speculate that the quantity of net lactate efflux from vascular beds with insufficient oxygen uptake exceeds the net influx into organs such as the liver, resulting in metabolic acidosis.

Acidosis↗
PubMed1994

Relationship between intracellular pH, extracellular pH, and ventilation during dilution acidosis.

Previous experiments showed that acute hyperosmolality results in an extracellular acidosis that does not stimulate respiratory compensation (C.E. Kasserra, D. R. Jones, and M. R. Hughes. Respir. Physiol. 85: 383-393, 1991). The data suggested that development of the extracellular dilution acidosis would also result in a concomitant intracellular contraction alkalosis. The effects of acute hyperosmolality and lactacidosis on systemic intracellular pH (pHi) were studied in the conscious Pekin duck in an effort to separate the effects of pHi and extracellular pH (pHe) on ventilatory control. Brain pH was also measured during systemic hyperosmolality to determine the relationship between blood and brain pHi. Hyperosmolality caused a concurrent extracellular acidosis and intracellular alkalosis in pectoral muscle, whereas lactic acid infusion decreased both pHe and pHi. Ventilation was stimulated only during lactacidosis and did not change during hyperosmolality. Brain pHi did not show a consistent significant increase in response to systemic hyperosmolality over 1 h but did show a trend toward an alkalosis. Measurement of high-energy phosphate metabolites (phosphocreatine, ATP, and Pi) indicated an increase of metabolic rate during hyperosmolality. With the assumption that similar pHi changes were occurring in chemoreceptive cells, the results suggest that ventilation was responding to pHi changes and that much of the depressive response to acute hyperosmotic disturbance was peripherally generated.

Acidosis, Lactic↗
PubMedDate not supplied

Lactic acidosis in asthma: report of two cases and review of the literature.

Lactic acidosis is commonly associated with states of hypoxia and decreased tissue perfusion. Elevated lactic acid levels have also been observed in individuals who are not septic and who are normotensive, but who have received systemic adrenergic agonist therapy. This report presents two patients with acute asthma treated with very large doses of aerosolized and systemic salbutamol, who developed lactic acidosis despite normal systemic hemodynamics and adequate oxygenation. Lactic acidosis was clinically important because it contributed to respiratory failure in one patient, and complicated the assessment and management of acute, severe asthma in the other patient.

Acidosis, Lactic↗
PubMed1998

Free circulating magnesium and renal magnesium handling during acute metabolic acidosis in humans.

Ion-selective electrodes have been designed for determining the ionized concentration of magnesium in blood, the biologically active form of this ion. The effect of acute acidosis induced by ammonium loading on circulating and urinary magnesium was investigated in 11 volunteers. No changes in plasma total and ionized magnesium were noted following administration of ammonium chloride. On the contrary, administration of ammonium chloride increased the plasma free magnesium fraction and the urinary magnesium excretion. The study demonstrates that the hypermagnesiuria induced by acute acidosis is not caused by ionized hypermagnesemia and supports the theory that acidosis decreases the circulating magnesium fraction that is bound to proteins.

Acidosis↗