Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0847097 (acidity)
 15,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was conducted to determine the effect of a high protein diet on calcium metabolism in rat. Wistar strain male rats (50 days old) were divided into 5 groups (day 0): control diet (18% casein); high protein diet (18% casein +20% lactalbumin); high protein and 0.1% sodium bicarbonate diet; high protein and 0.2% sodium bicarbonate diet; and high protein and 0.4% sodium bicarbonate diet. On days 0, 1, 3, 5, 7, 9, urine samples were collected and, at the same time, feces were collected from half of the animals in each group. Urinary titratable acidity (TA-HCO3-), ammonium ion (NH4+), and net acid excretion (NAE) were measured as an index of acid-base balance in rat body. Urinary volume was rapidly increased and the increase of urinary volume continued throughout the study in rats fed the high protein diet. Urinary excretions of calcium and phosphorus were increased after day 3 and day 1, respectively, in rats fed the high protein diet. The high protein diet depressed calcium absorption and elevated phosphorus absorption from the digestive tract in rats fed the high protein diet. The high protein diet decreased TA-HCO3-, which was closely correlated with the decrease of NAE. Sodium bicarbonate supplementation to the high protein diet had little effect on urinary calcium excretion and NAE. This study suggested that there was no relationship between metabolic acidosis and hypercalciuria in rats fed the high protein diet.
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PMID:Effects of high protein diet and sodium bicarbonate supplementation on calcium metabolism in rats. 263 82

Bismuth salts are successfully used for the treatment of campylobacter-pylori-associated gastritis. It cannot be excluded, however, that calcium carbonate, which is present in one of the recommended preparations (calcium carbonate/bismuth subsalicylate, Jatrox), may have an additional therapeutic effect due to an increase of intragastric pH. Therefore, the in-vitro H+ buffering capacity of Jatrox was determined in comparison to other antacids using the pH-stat technique, and its effect on intragastric acidity was tested in 15 healthy volunteers using ambulatory 24-hour pH-metry (combined glass electrode in gastric corpus, solid state memory recorder, sampling rate 30/min). At two study sessions, the volunteers received standardized normal meals (8:00 a.m., 12:00 noon, 6:00 p.m.) and, in randomized order, either Jatrox (three times 2 tablets one hour before meals) or no medication. Under in-vitro conditions, the buffering capacity of Jatrox amounts to 7.82 mmol H+ per tablet (equivalent to 47 mmol H+/24 h at recommended dosage), which is relatively low. Under in-vivo conditions, gastric pH only increases significantly during the first hour after medication. This short-lasting effect, however, has no influence on the 24-hour median pH. It is concluded from these results that the calcium carbonate contained in Jatrox probably does not contribute directly towards its therapeutic effect in promoting the healing of gastritis.
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PMID:[The effect of a calcium carbonate-bismuth subsalicylate combination on intragastric acidity over the course of 24 hours. A randomized study of healthy probands]. 271 11

This study systematically evaluates the effect of changes in the acid-base composition of the incubation media on the electrogenic H+ and HCO3- secretion (voltage clamp method and serosal ouabain) in the isolated turtle urinary bladder. Since the various cell types would change their acidity in a similar direction but to a variable degree, measured mean cell pH values (5,5-dimethyl-2,3-oxazolidinedione method) were used for an overall assessment of the changes in the acid-base status of the acid-transporting cells. Although addition of exogenous CO2 (0.7-3%) increased H+ secretion (JH+) 2- to 4-fold from a CO2-free control period, a further increase in the percent of CO2 did not enhance JH+ demonstrating a permissive but not a stimulatory role of CO2. Cyclic AMP plus 3-isobutyl-1-methylxanthine-induced electrogenic HCO3 secretion (JHCO3-) remained unaltered at 10% CO2 from a 5% CO2 control period. Cell acidosis resulting from either alterations in the PCO2/HCO3- levels or from NH4Cl in the bathing solution did not enhance JH+; by contrast maximal levels of acidification were found at cell pH values of about 7.40 and comparable effects on JH+ were found with a variety of PCO2/HCO3- combinations that led to a similar intracellular acidity.
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PMID:Marginal effect of changes in acid-base status in vitro on rheogenic H+ and HCO3- secretion in turtle urinary bladder. 283 10

The effects of different insufflation media gases for pneumoperitoneum on the acidity of follicular fluid and blood acid--base balance were studied in two groups of patients during laparoscopic oocyte retrieval. Insufflation with 100% CO2 was compared with insufflation with 5% CO2 in air. End-tidal CO2 and the acid-base status of arterial blood, follicular and Douglas fluids were evaluated. When using 5% CO2 in air as insufflation gas, pH values and pCO2 levels observed in the aspirated follicular (pH: 7.35 +/- 0.06, pCO2: 38.8 +/- 4.5 mmHg) and Douglas fluid (pH: 7.40 +/- 0.07, pCO2: 38.5 +/- 6.2 mmHg) remained normal. With 100% CO2 insufflation, the follicular fluid pH (7.22 +/- 0.07) and pCO2 (53.1 +/- 10.9 mmHg) and the Douglas fluid pH (6.99 +/- 0.12) and pCO2 (90.3 +/- 18.4 mmHg) were grossly disturbed and outside the physiological range. No differences occurred in pO2 or HCO3 levels. These data suggest that pneumoperitoneum with 5% CO2 in air provides more optimal environmental conditions for oocytes used for in-vitro fertilization. However, further investigations on large patient groups are required to demonstrate whether such environmental conditions influence the success rate of in-vitro fertilization in humans.
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PMID:Pneumoperitoneum induced pH changes in follicular and Douglas fluids during laparoscopic oocyte retrieval in humans. 285 15

It is uncertain whether, in humans, potassium depletion can cause or sustain metabolic alkalosis of clinically important degree in the absence of coexisting known alkalosis-producing conditions. Previously we found, in normal humans ingesting abundant NaCl, that dietary K+ depletion alone can induce and sustain a small decrease in blood acidity and increase in plasma bicarbonate concentration; we hypothesized that more severe alkalosis was prevented by mitigating mechanisms initiated by renal retention of dietary NaCl that was induced by K+ depletion. To ascertain the acid-base response to dietary K+ depletion under conditions in which the availability of NaCl for retention is greatly limited, in the present study of six normal men we restricted dietary K+ as in the previous study except that intake of NaCl was maintained low (2 to 7 mEq/day, Low NaCl Group) instead of high (126 mEq/day, High NaCl Group). Plasma acid-base composition and renal net-acid excretion (NAE) did not differ significantly between groups during the control period. In the steady state of K+ depletion (days 11 to 15 of K+ restriction), neither plasma K+ concentration (2.9 +/- 0.9 mEq/liter vs. 3.0 +/- 0.1 mEq/liter) nor cumulative K+ deficit (399 +/- 59 mEq vs. 466 +/- 48 mEq) differed significantly between groups. During K+ restriction, persisting metabolic alkalosis developed in both groups, which was more severe in the Low NaCl Group: increment in [HCO3-]p, 7.5 +/- 1.0 mEq/liter versus 2.0 +/- 0.3 mEq/liter, P less than 0.001; decrement in [H+]p, 5.5 +/- 0.6 nEq/liter versus 2.9 +/- 0.4 nEq/liter, P less than 0.003. A significantly more severe alkalosis in the Low NaCl Group was evident at all degrees of K+ deficiency achieved during the course of the 15 days of K+ restriction, and the severity of alkalosis in the Low NaCl Group correlated with the degree of K+ deficiency. During the generation of alkalosis (days 1 to 7 of K+ restriction), NAE increased in the Low NaCl Group whereas it decreased in the High NaCl Group. During the maintenance of alkalosis (days 11 to 15), NAE stabilized in both groups after it returned to values approximating the control values. In both groups, urine Cl- excretion decreased during K+ restriction even though Cl- intake had not been changed, with the result that body Cl- content increased negligibly in the Low NaCl Group (28 +/- 6 mEq) and substantially in the High NaCl Group (355 +/- 64 mEq).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Dietary NaCl determines severity of potassium depletion-induced metabolic alkalosis. 303 34

A randomized, prospective, crossing-over clinico-pharmacological study was conducted on the tolerability by humans, of TISACID (Al-Mg-hydroxy-carbonate), a new antacid of up-to-date composition produced in Hungary. Even a relatively high dose of the preparation is tolerated by the human organism. During a 6-week continuous treatment neither subjective nor objective side-effects were observed. The tablet is immediately decomposed in the gastric juice, a considerable portion of it will permanently stick to the mucosa of the stomach and duodenum. Depending on the dose, it rapidly and permanently reduces the acidity of the gastric content and increases serum gastrin concentration only moderately and for a short time. Administered together with cimetidine, it promotes healing of duodenal ulcer and the cessation of complaints. It does not increase the aluminium and magnesium concentrations of the plasma not even on prolonged administration, and clinical symptoms and laboratory changes characterizing the phosphate depletion syndrome do not develop either. Based on the results, authors consider Tisacid a beneficial preparation as regards both effectivity and tolerability.
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PMID:Human tolerability and pharmacodynamic study of Tisacid tablet in duodenal ulcer patients. A prospective, randomized, self-controlled clinicopharmacological study. 307 55

Acetazolamide (AZ) inhibition of brain and blood carbonic anhydrase increases cerebral blood flow by acidifying cerebral extracellular fluid (ECF). This ECF acidosis was studied to determine whether it results from high PCO2, carbonic acidosis (accumulation of H2CO3), or lactic acidosis. Twenty rabbits were anesthetized with pentobarbital sodium, paralyzed, and mechanically ventilated with 100% O2. The cerebral cortex was exposed and fitted with thermostatted flat-surfaced pH and PCO2 electrodes. Control values (n = 14) for cortex ECF were pH 7.10 +/- 0.11 (SD), PCO2 42.2 +/- 4.1 Torr, PO2 107 +/- 17 Torr, HCO3- 13.8 +/- 3.0 mM. Control values (n = 14) for arterial blood were arterial pH (pHa) 7.46 +/- 0.03 (SD), arterial PCO2 (PaCO2) 32.0 +/- 4.1 Torr, arterial PO2 (PaO2) 425 +/- 6 Torr, HCO3- 21.0 +/- 2.0 mM. After intravenous infusion of AZ (25 mg/kg), end-tidal PCO2 and brain ECF pH immediately fell and cortex PCO2 rose. Ventilation was increased in nine rabbits to bring ECF PCO2 back to control. The changes in ECF PCO2 then were as follows: pHa + 0.04 +/- 0.09, PaCO2 -8.0 +/- 5.9 Torr, HCO3(-)-2.7 +/- 2.3 mM, PaO2 +49 +/- 62 Torr, and changes in cortex ECF were as follows: pH -0.08 +/- 0.04, PCO2 -0.2 +/- 1.6 Torr, HCO3(-)-1.7 +/- 1.3 mM, PO2 +9 +/- 4 Torr. Thus excess acidity remained in ECF after ECF PCO2 was returned to control values. The response of intracellular pH, high-energy phosphate compounds, and lactic acid to AZ administration was followed in vivo in five other rabbits with 31P and 1H nuclear magnetic resonance spectroscopy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of acetazolamide on cerebral acid-base balance. 313 34

Acute metabolic acidosis potentiates the nephrotoxicity of aminoglycosides by impairing the adequate excretion of ammonium and titratable acidity. The present study assesses distal tubular function after aminoglycoside administration in the rat. Two aminoglycosides, gentamicin and netilmycin were given to rats either in low doses equivalent to those used clinically (BG4 and BN5 groups) or in doses ten times higher (BG40 and BN50). The rats were subjected to acute metabolic alkalosis and the pCO2 of urine was continuously evaluated. The regression lines obtained by plotting the differences between urine and blood pCO2 as a function of urinary HCO3- in low dose models were similar to those obtained for the control group. However, the slopes obtained for BG40 and BN50 were significantly different from the control, suggesting an impairment of H+ secretion.
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PMID:Evaluation of distal tubular function in aminoglycoside-induced nephropathy. 313 93

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)
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PMID:Interorgan glutamine flow in metabolic acidosis. 332 41

Tissue pH in the immediate subepithelial layer of rat gastric mucosa was measured using H+-selective microelectrodes. Exposure of the mucosa to luminal acid (50-150 mM) caused a significant acidification of the subepithelial tissue. Contrary to expectation, disruption of the mucosal barrier with taurocholate (10 mM), acetylsalicylic acid (10 mM), or ethanol (20% vol/vol) during acid (100 mM HCl) perfusion promoted no further acidification of the subepithelial tissue but rather caused an alkalinization of the primarily acidified subepithelial tissue. When hemorrhagic shock was induced during acid perfusion, a profound acidification of the subepithelial tissue occurred even though a much lower luminal acidity (10 mM HCl) was used. Also, taurocholate had no alkalinizing influence on subepithelial pH during hemorrhagic shock, but caused a rapidly progressing and irreversible drop of the subepithelial tissue pH. The findings suggest that in normal stomach with intact "mucosal barrier," H+ back-diffusion occurs during exposure to acid. However, disruption of the mucosal barrier seems to lead to alkali (HCO3-) efflux from the mucosa, which neutralizes the influxing H+, thus "masking" H+ back-diffusion and protecting the mucosa. Yet, when adequate supply of HCO3- to the mucosa is blocked during exposure to a barrier-breaking agent and acid, increased H+ back-diffusion becomes again "unmasked," leading to extensive acidification and ulceration of the mucosa.
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PMID:Subepithelial tissue pH of rat gastric mucosa exposed to luminal acid, barrier breaking agents, and hemorrhagic shock. 333 38


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