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

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.
 ...
PMID:Subepithelial tissue pH of rat gastric mucosa exposed to luminal acid, barrier breaking agents, and hemorrhagic shock. 333 38

We evaluated the importance of pH, titratable acidity, and specific chemical composition in acid aerosol-induced bronchoconstriction in 8 asthmatic subjects. We administered aerosols of HCl and H2SO4 at pH 2.0 in an unbuffered state and buffered with glycine. The buffered acids were given in order of increasing titratable acidity (defined as the number of ml of 1 N NaOH required to neutralize 100 ml of acid solution to pH 7.0). Each set of buffered or unbuffered acid aerosols was given on a separate day and each aerosol was inhaled through a mouthpiece during 3 min of tidal breathing. Bronchoconstriction was assessed by measurement of specific airway resistance (SRaw) before and after inhalation of each aerosol. SRaw increased by more than 50% above baseline in 1 of 8 subjects after inhalation of unbuffered HCl and in no subjects after inhalation of unbuffered H2SO4, even at pH 2.0. In contrast, SRaw increased by greater than 50% in all 8 subjects after inhalation of HCl and glycine at pH 2.0 and 7 of 8 subjects after inhalation of H2SO4 and glycine at pH 2.0. The mean titratable acidity required to increase SRaw by 50% above baseline was calculated for each challenge by linear interpolation; these values for H2SO4 and glycine (5.1 ml of 1 N NaOH) and HCl and glycine (2.2 ml of 1 N NaOH) were slightly, but significantly, different (p = 0.01) and were considerably higher than the titratable acidity of the unbuffered acids at pH 2 (1.0 ml of 1 N NaOH).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:The role of titratable acidity in acid aerosol-induced bronchoconstriction. 355 4

Two experiments of Latin square design, with four Friesian bull calves fitted with re-entrant duodenal cannulas at 4-10 d of age, were made to study the effect of giving varying levels of single-cell protein on the abomasal outflow and composition of digesta. In Expt 1, diets in which 0, 220, 440, and 660 g/kg milk protein were replaced by the bacterial protein Pruteen were compared from 14 d of age. In Expt 2, which began at about 61 d of age, a comparison was made of diets in which 0, 220, 440 and 660 g/kg milk protein were replaced by the yeast protein Toprina. Collection of abomasal outflow was made for 8 h after feeding for 2 d within each 6 d period of the Latin square design experiment. The amount of diet offered daily was 50 g dry matter/kg body-weight 0.75. Polyethylene glycol (PEG), which was used as an indigestible marker, total nitrogen (TN), protein-N (PN), fat, and potassium, sodium and chloride ion outflows were measured together with pepsin (EC 3.4.23.1) and chymosin (EC 3.4.23.4) activities, pH and titratable acidity. In Expt 1 there was little difference in the outflow of liquid digesta between diets and about 0.9 of the dietary PEG was recovered within the 8 h collection period. With increasing amounts of Pruteen in the diet, outflows of TN, PN, fat and Na+ increased, and the pH of digesta increased. However, the volume of 'apparent secretion' into the abomasum (outflow - intake), pepsin activity, chymosin activity, titratable acidity, (outflow of Cl- -outflow of Na+) as a measure of outflow of HCl, and outflows of K+ and of Cl- were reduced. All outflows decreased with the time interval after feeding, except (Cl- -Na+) outflow. In Expt 2, the same trends as in Expt 1 were apparent, but since one calf had to be slaughtered and the experiment had to be analysed as a randomized block, only PN and K+ outflows and pH were significantly affected by dietary treatment, with K+ outflow increasing, rather than decreasing, with increasing concentration of single-cell protein in the diet.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Digestion, absorption and utilization of single-cell protein by the preruminant calf. Abomasal outflow and its composition from calves given milk-substitute diets containing varying amounts of either bacterial or yeast protein. 393 53

The effect of cimetidine on gastric emptying and gastric secretion was evaluated in eight chair-adapted rhesus monkeys. A dye-dilution technique was used to simultaneously determine gastric emptying, gastric secretion of water and hydrogen ion (H+), and intragastric volume and H+ concentration. A continuous intravenous infusion of either saline (control) or cimetidine (4 mg X kg-1 X h-1) was administered during a 40-min fasting steady state and following intragastric instillation of 100 ml of water. During fasting, administration of cimetidine abolished H+ secretion and significantly decreased fractional emptying rate and water secretion (P less than 0.05). After the water load, cimetidine also suppressed H+ secretion and reduced fractional emptying and water secretion compared with control (P less than 0.05). Increasing HCl concentration of the test solution to 50 mM significantly decreased fractional emptying both during saline and further suppressed emptying during cimetidine infusion (P less than 0.05). In conclusion, cimetidine significantly decreased gastric emptying during fasting and following a liquid load. Restoring intragastric acidity to physiological levels removed the effect of gastric acid suppression on emptying and unmasked the full potential for cimetidine to decrease gastric emptying, possibily through an effect on gastric smooth muscle.
 ...
PMID:Histamine H2-receptor involvement in the regulation of gastric emptying. 395 4

1. The reversible NAD(+)-linked oxidation of d-3-hydroxybutyrate to acetoacetate in 0.1m-sodium pyrophosphate buffer, pH8.5, at 25.0 degrees C, catalysed by d-3-hydroxybutyrate dehydrogenase (d-3-hydroxybutyrate-NAD(+) oxidoreductase, EC 1.1.1.30), was studied kinetically at chemical equilibrium by monitoring radioisotope redistribution with sodium dl-hydroxy[3-(14)C]butyrate and [4-(3)H]NAD(+)(labelled in the nicotinamide ring). 2. When all substrates are maintained at concentrations approaching saturation (approx. 3-50 times the K(m) values) the first-order rate constant for the enzyme-catalysed interconversion of NAD(+) and NADH is much smaller than that for the enzyme-catalysed interconversion of d-3-hydroxybutyrate and acetoacetate. 3. The rate of interconversion of NAD(+) and NADH increases initially with increasing concentrations of d-3-hydroxybutyrate and acetoacetate (ratio of concentrations maintained constant), passes through a maximum and approaches closely to zero at saturating concentrations of the latter substrates. 4. The rates of interconversion of NAD(+) and NADH and of d-3-hydroxybutyrate and acetoacetate increase with increasing concentration of NAD(+) (up to 66 times its K(m) value) and NADH (up to 180 times its K(m) value) (ratio of the concentrations of the nicotinamide nucleotides maintained constant). 5. These findings support the description of this catalysis as an ordered Bi Bi mechanism with no detectable alternative pathway, in which the interconversion of the central ternary complexes is not rate-limiting, and provide no evidence for the formation of dead-end complexes. 6. The solubility of 2,4-dinitrophenylhydrazine in HCl exhibits an acidity optimum, the maximum solubility at 25.0 degrees C (3.8mg/ml, 19mm) occurring at 2.29m-HCl; in solutions of this acidity acetone 2,4-dinitrophenylhydrazone is relatively insoluble (0.098mg/ml, 0.413mm).
 ...
PMID:D-3-hydroxybutyrate dehydrogenase from Rhodopseudomonas spheroides. Kinetics of radioisotope redistribution at chemical equilibrium catalysed by the enzyme in solutions. 435 36

The influence of gastric acidity on the absorption of intragastrically administered fluoride was investigated in rats. Intact animals were pretreated with atropine or cimetidine to reduce gastric acid secretion or were given fluoride in NaHCO3 to reduce the acidity of the gastric contents. Compared with pentagastrin-treated animals or animals that received fluoride in 0.1 N HCl, their rate of fluoride absorption was markedly reduced as judged by lower plasma fluoride concentrations and areas under the time-plasma concentration curves, especially during the first hour after dosing. In crossover studies with the stomachs isolated in situ, fluoride absorption was at least 50% faster from a pH 2.1 buffer compared with its absorption from a pH 7.1 buffer. The findings are consistent with the hypothesis that fluoride is absorbed from the gastric lumen principally as the undissociated molecule, HF. The results may contribute to a more complete understanding of acute fluoride toxicity, the development of dental fluorosis and, perhaps, the use of fluoride in the treatment of osteoporosis.
 ...
PMID:Fluoride absorption: the influence of gastric acidity. 608 10

Studies have demonstrated that the protective effect of secondary hypocapnia on plasma acidity during chronic HCl-acidosis is undermined by a renal-mediated decrement in plasma bicarbonate concentration induced by the hypocapnia itself. The present study was designed to assess whether the protection of "whole body" intracellular pH (pHi) is similarly undermined by this maladaptive response of the kidney. Whole body pHi was estimated by the 5,5 dimethyl-2,4-oxazolidinedione (DMO) method in seven unanesthetized dogs under each of three conditions: control, chronic HCl-acidosis (10 mEq H+/kg/day) with spontaneous secondary hypocapnia, and chronic HCl-acidosis with a normal level of carbon dioxide tension (maintained by the use of an environmental chamber). pHi was 6.71 +/- 0.02 during control, and 6.57 +/- 0.03 and 6.57 +/- 0.02 during the two acidosis periods, respectively. These results indicate that sustained secondary hypocapnia fails to render the intracellular compartment less acidic because of a maladaptive reduction in intracellular bicarbonate concentration.
 ...
PMID:Secondary hypocapnia fails to protect "whole body" intracellular pH during chronic HCl-acidosis in the dog. 640 72

It is known that Pi normally provides the major source of non-NH3 urinary buffer and that Pi-buffered renal H+ excretion (titratable acidity, TA) accounts for a large fraction of daily renal net acid excretion (NAE). Whether the presence of luminal non-NH3 buffers is a prerequisite to normal renal regulation of systemic acid-base equilibrium under any conditions has not been investigated. Accordingly, I investigated whether chronic renal regulation of plasma (p) [HCO3] might be impaired under conditions of normophosphatemic hypophosphaturia (NHP) produced by short-term dietary Pi restriction. During a steady-state of HCl-induced acidosis in NaCl-replete NHP dogs (group 1A, N = 6), [HCO3-]p averaged 14.1 +/- 0.6 mEq/liter and arterial (a) [H+] averaged 54 +/- 2 nEq/liter. Substitution K+ 2.5 mEq/kg as neutral Pi for equivalent dietary KCl for 7 to 8 days resulted in significant amelioration of acidosis (delta [HCO3-]p + 2.2 +/- 0.5 mEq/liter, P less than 0.01; delta [H+]a -6 +/- 2 nEq/liter, P less than 0.01) in association with a cumulative increment (sigma delta) in TA excretion (+ 103 mEq, P less than 0.001) and NAE (+ 22 mEq). To investigate whether Pi-induced amelioration of acidosis was related to enhanced urinary buffer capacity, an additional group (group 1B, N = 5) with NHP and chronic HCl acidosis was administered the non-Pi buffer, neutral creatinine (5.0 mmoles/kg daily). As with Pi, acidosis was ameliorated by creatinine administration and sigma delta NAE increased.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Hypophosphaturia impairs the renal defense against metabolic acidosis. 651 76

A study was undertaken on the antiulcer effect of some active ingredients present in the lipid part of the fruits of M. azedarach administered p.o. to male rats. Acute gastric ulcers were induced by gipsing the rats for 22 hr preceded by 24 hr starvation to obtain the maximum stress. The free HCl, total HCl and total acidity were also measured. The total lipid (TLP), 1.0, 2.5 and 5.0 g/kg, reduced the ulcer index by 25-41.8% and 50-58% when given daily for 5 and 10 days, respectively. The saponifiable fraction (SP), 0.85, 2.0 and 4.0 g/kg, given for 10 days reduced the ulcer index by 41.8-50%, while the nonsaponifiable (NSP), 0.075, 0.150 and 0.50 g/kg, for 10 days reduced it by 50-83.5%. The 70% ethanol extract of the defatted residue showed no antiulcer effect. Analysis of the gastric juice showed a significant decrease in free HCl (P less than 0.001) induced by TLP; the total HCl and total acidity were reduced only at 5 g/kg. The results revealed the antiulcer effect of the lipid components of M. azedarach fruits which is mainly due to the phytosterol fraction.
 ...
PMID:Effect of Melia azedarach fruits on gipsing-restraint stress-induced ulcers in rats. 654 33

Gastric ulcerations were produced in rats by oral administration of aspirin (ASA) suspended in a vehicle consisting of either water or increasing concentrations of HCl (0.005 M to 0.35 M). The lesions were prevented by antisecretory doses of a histamine H2 blocker (cimetidine) and by an anticholinergic agent (pro-banthine), but only when the acidity of the vehicle was low (0.05 M to 0.15 M), not at higher (0.35 M). On the other hand, 16,16-dimethyl PGE2 prevented ulcer formation even when ASA was suspended in all HCl concentrations, including 0.35 M HCl. In other studies, gastric mucosal necrosis was produced by oral administration of absolute ethanol. These lesions were not affected by cimetidine or two anticholinergic agents, pro-banthine and methscopolamine bromide, nor by alkalinization of the gastric lumen with NaHCO3 or pH 7 buffer; however, these ethanol-induced lesions were completely prevented by 16,16-dimethyl PGE2. We conclude that antisecretory agents, by blocking endogenous formation of acid, are antiulcer as long as no acid or only small amounts of acid (1 ml of 0.15 M or less) are given together with ASA. When higher concentrations are used (e.g. 0.35 M HCl), the antisecretory effect of the inhibitors is overcome by the exogenous acid, and ulcers still form. Under these conditions, only "true" cytoprotective agents, such as 16,16-dimethyl PGE2, prevent ASA-induced ulcers, even in the presence of high acidity. Although cimetidine and pro-banthine were shown earlier to reduce ASA-induced ulcers at nonantisecretory doses, these agents may still decrease acid formation within the gastric glands.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Distinction between antiulcer effect and cytoprotection. 659 40


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>