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PubMedDate not supplied

Inhibitory action of peptide YY on pancreatic secretion is independent of secretin.

The purpose of this study was to characterize the effect of peptide YY (PYY) on acid-stimulated pancreatic bicarbonate secretion and to determine whether PYY affects the release of secretin in response to intraduodenal infusion of acid. Six dogs were prepared with gastric and pancreatic cannulas. In study 1, graded doses of hydrochloric acid (HCl) (3, 6, 12, and 24 mEq/h) were given intraduodenally alone or in combination with intravenous PYY (400 pmol/kg.h). In study II, and ED50 of intraduodenal HCl (6 mEq/h) was given alone or in combination with graded doses of PYY (12.5, 25, 50, 100, 200, and 400 pmol/kg.h, i.v.). Bicarbonate output was significantly inhibited during PYY infusion at 200 and 400 pmol/kg.h, but plasma secretin levels were unchanged. The calculated maximal response for bicarbonate secretion (5.1 +/- 1.3 mEq/15 min) was significantly reduced by PYY (2.1 +/- 0.7 mEq/15 min). We concluded that PYY can inhibit acid-stimulated pancreatic bicarbonate secretion without affecting the release of secretin. The mechanism of the inhibitory effect of PYY on acid-stimulated pancreatic bicarbonate secretion is compatible with a noncompetitive type of inhibition.

Animals↗
PubMed1988

The dissolution rate of enamel in acid in developing rat incisors.

This study was undertaken to determine the changes in this dissolution rate at different developmental stages after different fluoride dietary regimes. Four groups of Wistar rats received water with 0, 25, 50 and 100 parts/10(6) fluoride respectively for 10 weeks. Six exposed windows of 2 mm2 were prepared on the enamel surface of the upper incisors, corresponding to six different developmental stages. The acid-dissolution rates were determined at each window by using 1.4 M sodium acetate-hydrochloric acid buffer (pH 2.3). The rate of enamel dissolution was highest in the matrix-formation stage and dropped sharply in a step-wise fashion towards the stages of secondary mineralization and iron deposition. The dissolution rate in the maturation stage decreased significantly with increasing intake of fluoride. However, in the pigmented enamel, the opposite occurred. The iron pigmentation or the porosity in this region of fluorosed enamel might be responsible for the change in the dissolution rate of the pigmented enamel.

Animals↗
PubMed1981

Angiotensin I recovery from plasma incubated with organic reagents.

(1) In order to explore the possible mechanism that organic reagents used in the incubation step of the plasma renin activity (PRA) analysis act as a angiotensinase inhibitors we did angiotensin I (AI) recovery studies from plasma with such reagents. The organic acids and their mean difference in percent recovery of AI as compared to that for hydrochloric acid (HCI) are respectively as follows for one and a three hour incubation time: maleic (0.7%, 4.5%); and potassium hydrogen phthalate (KHphthalate) (7.2%, 9.6%). The tris(hydroxymethyl)aminomethane (Tris) organic acid salts and their mean difference in percent recovery of AI as compared to that for Tris-HCl are as follows for a one hour incubation: Tris-acetylsalicylate (3.6%), Tris-phenoxyacetate (3.6%), Tris-benzoate (2.6%), and Tris-salicylate (4.9%). (2) Of the reagents studied KHphthalate after a three hour incubation produced a statistically significant difference from the HCl reagent. The recovery data for all the organic reagents suggested that the primary mechanism of action was not that of an angiotensinase inhibitory one.

Angiotensin I↗
PubMed1984

Histamine and slow reacting substance in acid-induced pneumonitis.

Acid pneumonitis was produced in 18 dogs by the tracheal instillation of 3 ml/kg 0.1 N hydrochloric acid. Arterial and mixed venous oxygen tension, static compliance and pulmonary capillary wedge pressure were measured during a 2-hour observation period. Plasma histamine (measured by the enzymatic isotopic assay) increased from 1.7 +/- 0.2 ng/ml (mean +/- SE) before acid injury to 13.5 +/- 1.9 ng/ml after injury (p less than 0.05). In one group of 7 control dogs, 3 ml/kg of normal saline produced no increase in plasma histamine. Pulmonary edema secretions from acid injured animals had a histamine level of 30.3 +/- 3.8 ng/ml and slow reacting substance was detected in 7 of 11 animals. The slow reacting substance was an antihistamine-resistant, ethanol extractable substance that contracted guinea pig ileum. Lung weight-body weight ratio PaO2, and static compliance were different with acid pneumonitis compared to controls. Total protein was not different in the tracheal secretions compared to plasma. We conclude that histamine and slow reacting substance are released in this animal model of acid pneumonitis and may be important in the pathogenesis of the lung injury.

Animals↗
PubMed1989

Gastric resistance to acid: is the "mucus-bicarbonate barrier" functionally redundant?

The functional importance of the "mucus-bicarbonate barrier" in protecting the gastric mucosa against injury by acid or pepsin was examined using an ex vivo gastric chamber preparation in the rat. Conditions were created such that the effectiveness of a mucus-stabilized pH gradient on the mucosal surface would be minimized. Thus solutions of hydrochloric acid of pH 1.3 or 0.8 were applied to the mucosal surface and continually stirred for 60 min. By use of an antimony pH microelectrode, these concentrations of acid were shown to dissipate the pH gradient on the mucosal surface within 5 min. The effects of addition of the mucolytic agents, pepsin or N-acetylcysteine, to both acid solutions were also assessed. Finally, the ability of the mucosa to resist injury by acid after disruption of the surface epithelium (with hypertonic saline) was examined. Exposure to the acid solutions, with or without added mucolytic agents, was without damaging effects on the mucosa, as assessed macroscopically, histologically, or by measurement of transmucosal potential difference and luminal protein concentration. Conversely, disruption of the surface epithelium rendered the mucosa significantly more susceptible to the damaging actions of acid. These results therefore demonstrate that under conditions in which a pH gradient on the mucosal surface was no longer detectable, the mucosa was resistant to injury by acid. In the undamaged rat stomach, therefore, the mucus-bicarbonate barrier may be functionally redundant.

Acetylcysteine↗
PubMed2003

Tracheobronchial stenosis from acid aspiration presenting as asthma.

We report a case of a 42-year-old man who fell in a vat of hydrochloric acid, resulting in ingestion and aspiration of acid. Initially, he suffered from a chemical pneumonitis and GI burns. He was released from the hospital without complications, only to return with signs and symptoms consistent with asthma. Evaluation revealed multiple areas of large airway stenosis, resulting from the chemical burns. The stenoses were treated with multiple stents.

Accidents, Occupational↗
PubMed1955

The inactivation of dilute solutions of crystalline trypsin by x-radiation. II. Effects of enzyme concentration, medium, pH, and temperature.

The proteolytic activity of dilute solutions of clystalline trypsin is destroyed by x-rays, the amount of inactivation being an exponential function of the radiation dose. The reaction yield increases steadily with increasing concentration of trypsin, varying, as the concentration of enzyme is increased from 1 to 300 microM, from 0.068 to 0.958 micromole of trypsin per liter inactivated per 1000 r with 0.005 N hydrochloric acid as the solvent, from 0.273 to 0.866 with 0.005 N sulfuric acid as the solvent, and from 0.343 to 0.844 with 0.005 N nitric acid as the solvent. When the reaction yields are plotted as a function of the initial concentration of trypsin, they fall on a curve given by the expression Y alpha X(K), in which Y is the reaction yield, X is the concentration of trypsin, and K is a constant equal to 0.46, 0.20, and 0.16, respectively, with 0.005 N hydrochloric, sulfuric, and nitric acids as solvents. The differences between the reaction yields found with chloride and sulfate ions in I to 10 microM trypsin solutions are significant only in the pH range from 2 to 4. The amount of inactivation obtained with a given dose of x-rays depends on the pH of the solution being irradiated and the nature of the solvent. The reaction yield-pH curve is a symmetrical one, with minimum yields at about pH 7. Buffers such as acetate, citrate, borate and barbiturate, and other organic molecules such as ethanol and glucose, in concentrations as low as 20 microM, inhibit the inactivation of trypsin by x-radiation. Sigmoid inactivation-dose curves instead of exponential ones are obtained in the presence of ethanol. The reaction yields for the inactivation of trypsin solutions by x-rays are approximately 1.5 times greater when the irradiation is done at 26 degrees C. than when it is done at 5 degrees C., when 0.005 N hydrochloric acid is the solvent. The dependence on temperature is less when 0.005 N sulfuric acid is used, and is negligible with 0.005 N nitric acid. The difficulties involved in interpreting radiation effects in aqueous systems, and in comparing the results obtained under different experimental conditions, are discussed.

Buffers↗
PubMed1991

[Effects of ibuprofen and OKY-046 on ventilation perfusion distribution in acute respiratory failure].

Hydrochloric acid was injected into the trachea to produce acute respiratory failure in 18 anesthetized dogs. Six dogs were pretreated with ibuprofen (12.5 mg/kg), six dogs were given OKY-046 (0.5 mg/kg), and the remaining six were taken as controls. Distribution of ventilation-perfusion was evaluated by inert gas elimination technique. Acid aspiration caused a prompt decline in PaO2 with an increased perfusion to shunt and low VA/Q lung regions. Pretreatment with ibuprofen reduced pulmonary blood flow to shunt and low VA/Q regions for the first 2 hours after acid aspiration and attenuated hypoxemia, causing an increase in PVR. However, OKY-046, a thromboxane synthetase inhibitor, did not ameliorate acid-induced VA/Q mismatching and hypoxemia.

Animals↗
PubMed2005

Erosive effects of different acids on bovine enamel: release of calcium and phosphate in vitro.

The present study intended to investigate minimal erosive effects of different acids on enamel during short time incubation via determination of calcium and phosphate dissolution. Bovine enamel specimens were eroded for 1-5 min with eight different acids of pH 2, 2.3 and 3 (citric (CA), maleic (MA), lactic (LA), tartaric (TA), phosphoric (PA), oxalic (OA), acetic (AA) and hydrochloric acid (HCl)). Calcium (Ca) and phosphate (P) release were determined photometrically using arsenazo III (calcium) and malachite green (phosphate) as substrates. Each subgroup contained eight enamel specimens. Amount of titratable acid was determined for all acidic solutions. MA, LA, TA, AA and HCl caused linear release of Ca and P, PA of Ca, CA of P. For CA, MA, LA, TA, AA, PA and HCl mineral loss was shown to be pH-dependent. Ca dissolution varied between 28.6+/-4.4 (LA, pH 2) and 2.4+/-0.7 nmol mm(-2)min(-1) (HCl, pH 3), P dissolution ranged between 17.2+/-2.6 (LA, pH 2) and 1.4+/-0.4 nmol mm(-2)min(-1) (HCl, pH 3). LA was one of the most erosive acids. AA was very erosive at pH 3. HCl and MA were shown to have the lowest erosive effects. There was only a weak correlation (r=0.28) between P and Ca release and the amount of titratable acid. The method of the present study allows investigation of minimal erosive effects via direct determination of P and Ca dissolution. During short time exposition at constant pH level, erosive effects mainly depend on pH and type of acid but not on amount of titratable acid.

Acetic Acid↗
PubMed2006

PEEP has beneficial effects on inflammation in the injured and no deleterious effects on the noninjured lung after unilateral lung acid instillation.

OBJECTIVE: In clinical lung injury areas of inflammation and structural alveolar alteration are unevenly distributed and interspaced between healthy or less injured lung areas. Positive end-expiratory pressure (PEEP) applied with mechanical ventilation (MV) may affect injured and healthy lung areas differently. We compared the effects of PEEP on the inflammatory response in injured and noninjured regions of the lung in an animal model of unilateral lung acid instillation. SUBJECTS: Anesthetized, paralyzed, and ventilated rats. INTERVENTIONS: Rats underwent left-endobronchial instillation with either hydrochloric acid or isotonic saline and were randomized 24 h later to MV using constant tidal volume (16 ml/kg) with either ZEEP, PEEP at 5 mmHg, or PEEP at 10 mmHg. After 4 h of MV the animals (n=9 or 10 per group) were killed and inflammatory markers assessed in left- and right-lung lavage fluid samples. In four additional animals per group differential lung perfusion was assessed. RESULTS: Unilateral acid injury alone worsened oxygenation, decreased left-lung perfusion, and increased left-lung lavage neutrophil and macrophage counts and cytokine levels. MV with ZEEP further impaired oxygenation and further decreased left-lung perfusion in acid-injured animals. MV with high PEEP preserved oxygenation and significantly decreased left-lung lavage protein content and cell counts in acid-injured animals and had no deleterious effect on the right (noninjured) lung. CONCLUSION: In this model of unilateral lung acid injury high PEEP attenuates the inflammatory cell response in the acid-injured lung, preserved oxygenation and has no deleterious effects in the opposite lung.

Administration, Inhalation↗
PubMed2004

Effects of granulocyte colony-stimulating factor (G-CSF) and neutrophil elastase inhibitor (ONO-5046) on acid-induced lung injury in rats.

It has been suggested that neutrophils play an important role in acid-aspirated lung injury. We examined the effects of the high dose of granulocyte-colony stimulating factor (G-CSF), which is capable of increasing peripheral neutrophils, and a specific neutrophil elastase inhibitor (ONO-5046) on acid lung injury in rats. Animals were anesthetized and normal saline (NS, 2 mL kg(-1)) or hydrochloric acid (HCl, 0.1 N 2 mL kg(-1)) was then instilled into trachea. Thirty minutes before HCl instillation, G-CSF (150 microg kg(-1)) was injected subcutaneously or ONO-5046 (10 mg kg(-1) h(-1)) was infused continuously into the right jugular vein. Animals were ventilated during the experiments. Five hours after HCl or NS instillation, bronchoalveolar lavage fluid (BALF) and lung tissue samples were obtained. Total nuclear cell count, absorbance, albumin, tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, cytokine-induced neutrophil chemoattractant (CINC), neutrophil elastase in BALF, wet-to-dry (W/D) ratio were measured. HCl aspiration markedly increased these values in BALF and W/D ratio. Both ONO-5046 and G-CSF attenuated the parameters increased by acid-induced lung injury in rats. The data suggests that neutrophils play an important role in acid-induced lung injury. However, high-dose G-CSF does not exacerbate acid-aspirated lung injury in rats, although this agent causes an increase in peripheral neutrophils.

Animals↗
PubMed1987

The effect of acid perfusion on mucosal blood flow and intramural pH of rabbit duodenum.

To evaluate the role of blood flow for acid tolerance of the duodenal mucosa, we perfused the duodenums of anesthetized rabbits with different concentrations of hydrochloric acid (HCl). Acid perfusion stimulated blood flow to the duodenal wall in a concentration-dependent fashion up to 80 mmol/L HCl (0 mmol/L; 0.44 +/- 0.05, 10 mmol/L; 0.84 +/- 0.14, 50 mmol/L; 1.44 +/- 0.11, 80 mmol/L; 2.03 +/- 0.12, 100 mmol/L; 1.82 +/- 0.07 ml/gm/min X +/- SEM). The pH in the lamina propria of the mucosa, which was measured with antimony microelectrodes was not changed in experiments during perfusion with 50 and with 80 mmol/L HCl in normotension. Acidosis in the lamina propria could be demonstrated only when the duodenum was perfused with 100 and with 80 mmol/L HCl combined with hemorrhagic hypotension. Damage to the mucosa, which developed after 30 and 60 minutes of acid perfusion, also showed a H+-dependent pattern. Reduction of blood flow by hemorrhagic hypotension aggravated the morphologic damage. We conclude that luminal acid stimulates blood flow in the duodenum. The decrease in blood flow induced by hypotension results in a greater susceptibility to mucosal damage.

Animals↗
PubMed1992

Structural studies on bio-active compounds. Part 21. Acid-promoted debenzylations in antitumour 2,4-diamino-5-[4-(N-alkylbenzylamino)-3-nitrophenyl]-6-ethylp yrimidines.

Methylbenzoprim and ethylbenzoprim undergo debenzylation in hydrochloric acid. Two reaction mechanisms are proposed to explain this reaction, both of which involve a neighbouring group participation by the nitro group ortho to the tertiary amine fragment. The physical stability of dihydrofolate reductase inhibitors in the benzoprim class may influence the choice of a clinical candidate.

Aniline Compounds↗
PubMed1983

Concentrated albumin does not affect lung edema formation after acid instillation in the dog.

Recent investigations of the role of large infusions of concentrated serum albumin on the acute pulmonary edema caused by hydrochloric acid (HCl) aspiration have produced contradictory results. We used the open thorax anesthetized dog with weighed lung lobe as well as completely isolated perfused weighed lobes. The results were the same with both preparations. Instillation of 0.1 N HCl (2 ml/kg) caused small increases in pulmonary artery pressure, and the rate of lung weight gain increased from 1.2 to 2.5 g/h to 22.2 to 30.2 g/h. Addition of 25% human serum albumin, either before or after acid instillation, had no significant effect on the rate of lobe weight gain. Additional experiments showed that after HCl the rate of lobe weight gain was exquisitely sensitive to pulmonary arterial pressure. Albumin therapy is without benefit in the prevention or treatment of the pulmonary edema caused by HCl aspiration.

Animals↗
PubMed1978

Gastric emptying of ingested acid and its effects on plasma gastrin and secretin in duodenal ulcer subjects.

Abnormal acid production or handling is thought to be involved in duodenal ulceration. Gastric emptying of 25 mmol hydrochloric acid (250 ml 0.1 M solution) was studied by using an isotopic method in control and ulcer subjects. Plasma gastrin and secretin levels were simultaneously measured. Gastric emptying was significantly faster in ulcer subjects using several parameters. Plasma gastrin levels were suppressed in both groups, with equivocal differences between them. Mean plasma secretin levels showed no significant elevation in controls and at only one point in ulcer subjects. Mean elevation in plasma secretin levels during intermediate phase of gastric emptying (T30-70) correlated with rate of acid loss from stomach in both groups. Regression lines were significantly different in position, however, and indicated a higher threshold for secretin release in ulcer subjects. The significance of this in the pathogenesis of duodenal ulcer is discussed.

Adult↗
PubMed2006

Acid inactivation of prions: efficient at elevated temperature or high acid concentration.

Scrapie prion rods isolated from hamster and non-infectious aggregates of the corresponding recombinant protein rPrP(90-231) were incubated with hydrochloric acid. The amount of PrP and of infectivity that survived incubation in HCl at varying times, acid concentrations and temperatures was quantified by Western blot densitometry and bioassays, respectively. Prion rods and rPrP aggregates showed similar HCl hydrolysis kinetics of PrP, indicating structural homology. For 1 M HCl and 25 degrees C, the rate of PrP hydrolysis follows first-order kinetics at 0.014 h(-1); the rate of infectivity inactivation is 0.54 h(-1). Hydrolysis for 1 h at 25 degrees C was only slightly proportional to HCl concentration up to 5 M, but complete loss of infectivity and PrP reduction to <2 % was observed at 8 M HCl. The temperature dependence of unhydrolysed PrP, as well as infectivity at 1 M HCl for 1 h, showed a slight decrease up to 45 degrees C, but a sigmoidal decrease by several orders of magnitude at higher temperatures. The slow hydrolysis of PrP and inactivation of infectivity by acid treatment at room temperature are attributed to solvent inaccessibility of prion rods and rPrP aggregates, respectively. The more effective hydrolysis and inactivation at temperatures above 45 degrees C are interpreted as thermally induced disaggregation with an activation energy of 50-60 kJ mol(-1). Most importantly, infectivity was always inactivated faster or to a higher extent than PrP was hydrolysed at several incubation times, HCl concentrations and temperatures.

Animals↗
PubMed1975

The amino acid sequence of cerexin A (studies on antibiotics from the genus Bacillus. VII.

N-Bromosuccinimide cleavage reaction on cerexin A liberated allo-isoleucine. Treatment with conc. hydrochloric acid cleaved the antibiotic into two peptide fragments selectively at gamma-hydroxylysine residue. Deacylation with an enzyme preparation from Pseudomonas sp. afforded deacyl cerexin A. The amino acid sequences of these peptide fragments were examined by Edman degradation. From all the results, the entire amino acid sequence of cerexin A was deduced.

Amino Acid Sequence↗