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At least 145 records · Page 8Linked to original sources

Effects of hydrochloric acid on the development of enterochromaffin-like (ECL) cell hyperplasia in the rat stomach induced by omeprazole.

In the present study, gastric pH was lowered by hydrochloric acid to investigate whether the cause of enterochromaffin-like (ECL) cell hyperplasia was due to the inhibition of acid secretion by omeprazole or due to the direct action of the drug. Omeprazole was given to female Crj:CD (SD) rats in a daily oral dose of 2 or 8 mg/kg for 13 weeks, and 20 ml/kg of 0.12 N HCl was further given orally to the animals 3 and 6 hours after each dosing. The animals were killed at the end of the dosing period, and the stomach was removed and weighed. The thickness of the gastric wall was measured and ECL cell count and area rate of the cells were calculated with an image analyzer. There were no effects of the treatment with HCl on stomach weight or thickness of the gastric wall, but ECL cell count and area rate of the cells decreased markedly by the treatment with HCl. Therefore, the cause of gastric ECL cell hyperplasia induced by omeprazole was suggested to be sustained high gastric pH levels.

Animals↗

[The behaviour of codeine and codeine-6-glucuronide in hydrolysis with hydrochloric acid (author's transl)].

The behaviour of codeine and codeine-6-glucuronide with hydrochloric acid has been investigated. Three methods of hydrolysis were selected; they are often used in routine identification of drugs in urine. With method I (12--13% HCl; 30 min at 100 degrees C) about 53% of codeine-6-glucuronide were not hydrolized. The corresponding values: with method II (20% HCl; 6 min heated azeotrope in open vessel) about 8% and with method III (nearly 5% HCl; 30 min at 100 degrees C) about 83%.

Chemical Phenomena↗

Distribution of orally ingested hydrochloric acid in the thoracoabdominal cavity after death.

The authors encountered a case of hydrochloric acid (HCl) poisoning, thought to be caused by oral ingestion of concentrated HCl. Coagulation of the surface of the tongue and the mucosa of the pharynx, esophagus, and stomach were observed at forensic autopsy. An overabundance of Cl- was found in the gastric contents, corresponding to 8.19 mL of concentrated HCl. This was suggested to be a lethal oral dose of concentrated HCl, and the cause of death was determined to be HCl poisoning. Measuring the pH and concentrations of various ions in body fluids and contents of the alimentary tract enabled postmortem diffusion of HCl to be determined.

Abdominal Cavity↗

Hydrochloric acid for treating metabolic alkalosis.

Six patients with severe metabolic alkalosis were treated with intravenous hydrochloric acid (HCl) infusion. HCl was given through a central venous catheter, at a concentration of 0.1 mEq per ml. At least two of the following criteria were considered for initiation of the therapy: An arterial pH of greater than 7.45, a base excess (BE) of greater than +7 mmol/L, a PaCO2 of greater than 50 mmHg. The HCl amount was calculated using the BE formula, however, two thirds was infused for avoiding excessive acid loading. Patients were monitored by the blood gases, serum electrolytes, hemoglobin, hematocrit, bilirubin determinations and blood smear findings. While a significant decrease was noticed in pH and BE values, moderate changes were detected in PaCO2 due to different ventilatory status of the cases. All laboratory test results remained within normal limits and no complication was encountered. The advantage of the therapy is that less volume is needed for the correction of alkalosis, particularly in the cases requiring fluid restriction. HCl therapy, moreover, is a safe and time-saving method because of having rapid response to the treatment in the critically ill surgical patients.

Acid-Base Equilibrium↗

Acute myocardial infarction after hydrochloric acid ingestion.

We report a case of acute ST segment elevated myocardial infarction associated with hydrochloric acid ingestion. Severe systemic acidosis developed shortly after massive hydrochloric ingestion; it was complicated by the presence of acute myocardial infarction. A new complication of acid ingestion is presented and a possible mechanism is discussed.

Acidosis↗

Morphological changes in putrefactive anaerobe 3679 (Clostridium sporogenes) induced by sorbate, hydrochloric acid, and nitrite.

Putrefactive anaerobe 3679 (Clostridium sporogenes), a gram-positive bacterium, was examined by light and electron microscopy during normal growth and in a medium containing sorbate (50 mM, pH 6.5), hydrochloric acid (pH of medium adjusted from 7 to 5 with HCl), or nitrite (1 mM, pH 7). During the early exponential growth phase, untreated cells were filamentous and nonseptate, but became septate later and divided when the culture entered the stationary phase. Untreated short and filamentous cells had a double-layered cell wall. Sorbate-treated cells were usually filamentous and nonseptate, but with distorted shapes characterized by numerous bends and bulges. Septation, when present, resulted in minicells. The inner cell wall appeared to be thickened and the outer wall was absent in many areas. Acid-treated cells were similar to sorbate-treated cells but contained septa. Considerable cellular debris was present in the suspension. Nitrite-treated cells were also filamentous, bent, and bulged but the cell wall appeared normal. Considerable cellular debris was also present in suspensions of nitrite-treated cells. Changes in morphology are discussed in relation to possible mechanisms of cell growth regulation and the inhibitory action of sorbate, acid, and nitrite.

Cell Wall↗

Effects of dietary hydrochloric acid on voluntary food intake and metabolism of sheep in relation to the use of mineral acids as silage additives.

1. In Expt I, a pelleted grass-meal diet was supplemented with hydrochloric acid, added to the grass pellets before feeding, at five levels from 0 to 628 mmol/kg dry matter (DM). Each diet was offered ad lib. for 21 d to five sheep in a 5 x 5 Latin-square design. 2. Voluntary food intake decreased rectilinearly with increasing HCl supplementation (P less than 0.001), to 42% of the control value for sheep on the high-HCl diet. The decrease in food intake was related both to dietary pH and to the extent of metabolic acidosis induced by the HCl treatment. Although the pH of rumen fluid decreased slightly with increasing HCl supplementation, effects of the HCl treatment on volatile fatty acid concentrations in rumen fluid were not significant (P greater than 0.05). 3. In Expt 2, palatability and metabolic effects of dietary HCl were studied by comparing its effect when mixed into the pelleted grass meal before feeding, with and without a supplement of an equivalent amount of sodium bicarbonate given intraruminally, or when HCl was given intraruminally while the sheep consumed pelleted grass meal alone. Each of the three treatments was given at two levels of HCl, 280 and 560 mmol/kg DM. At each level of dietary HCl supplementation, the three treatments and the control diet (pelleted grass meal alone) were each given to four sheep, in a Latin-square design, for 11 d. 4. At the low level of supplementation, HCl, when mixed into the pelleted grass meal, reduced food intake by 17%, this effect was not altered by NaHCO3 supplementation, but when HCl was given intraruminally food intake was not reduced. At the high level of HCl supplementation, food intake was reduced by about 40% by each method of HCl supplementation; and NaHCO3 supplementation did not appreciably alter the effect of HCl on food intake, but prevented metabolic acidosis associated with the HCl treatments. Food intakes for the low-HCl treatments were significantly higher than those for the high-HCl treatments (P less than 0.01) and the level of dietary HCl x treatment interaction was also significant (P less than 0.01). DM digestibility, and the pH and volatile fatty acid concentrations of rumen fluid were not significantly affected by the different treatments. 5. It is concluded that at a low level of HCl supplementation the adverse effects of dietary HCl on voluntary food intake of sheep is determined by palatability associated with low dietary pH, whereas at a high level of HCl supplementation the effect is determined by palatability and by a metabolic response.

Acidosis↗

[Behaviour of hydroxymethyl-methaqualone-glucuronide in hydrolysis with hydrochloric acid (author's transl)].

The behaviour of the glucuronide derivative of 2'-hydroxymethylmethaqualone with hydrochloric acid was investigated. Three methods of hydrolysis were selected. With method I(12-13% HCl; 30 min at 100 degrees C) about 27% and with method II (20% HCl; 6 min heated azeotrope in open vessel) about 94-95% of the glucuronide derivative was hydrolyzed. With method III (approx. 5% HCl; 30 min at 100 degrees C) only about 3% of the conjugated compound was converted to the free form.

Glucuronates↗

A potential mechanism of action of colloidal bismuth subcitrate: diffusion barrier to hydrochloric acid.

The mode of action of colloidal bismuth subcitrate (CBS), a colloidal bismuth preparation often used in the treatment of gastroduodenal ulcers, is unknown. The precipitation characteristics of CBS were determined by titration with hydrochloric acid and gastric juice. The precipitation pH were 4.0 and 3.5 respectively. Preoperative administration of CBS resulted in a preferential accumulation of bismuth in chronic gastric ulcers as determined by tissue bismuth assays. CBS and gastric glycoprotein formed an in vitro complex which markedly retarded the migration of H+. One of the mechanisms by which CBS promotes ulcer healing is through its behaviour as a diffusion barrier to hydrochloric acid.

Anti-Ulcer Agents↗

Airway aspiration of hydrochloric acid in sheep.

We have compared the effects of aspiration of 2.5 ml/kg of 0.1 N hydrochloric acid (HCl) on groups undergoing normal saline aspiration (2.5 ml/kg) and a sham control in unanesthetized sheep with chronic lung lymph fistula for up to 148 hr. Significant changes in pulmonary lymph flow and cardiopulmonary variables occurred in the airway acid group within the first 48 hr, as compared to saline and sham control. In the HCl group lymph flow increased from a baseline of 8.5 +/- 1.5 to 21.8 +/- 3.0 ml/hr (mean +/- SEM) at 2 hr. Pulmonary vasoconstriction occurred at this time with significant elevations of lymph thromboxane B2 from a baseline of 400 +/- 11 to 2,090 +/- 690 pg/ml. During the early acid aspiration phase products of lipid peroxidation were noted to increase from 0.29 +/- 0.03 to 0.81 +/- 0.17 absorbance units. Associated with elevated lymph flow was a significant drop in cardiac index in the airway-acid-aspirated group (6.59 +/- 0.52 to 5.53 +/- 0.36 L/min/m2) and a rise in bronchial blood flow from 9.8 +/- 1.7 to 63.7 +/- 8.9 ml/min. These data suggest that a moderate airway acid injury created by 2.5 ml/kg of HCl results in acute pulmonary damage with the release of several potential mediators which may be responsible for the observed effects. The long-term acid-injured animals survived for up to 1 week following the aspiration procedure with evidence of resolution of lung damage by wet-weight dry-weight evaluation of lung (normal lab control = 4.0 +/- 0.2, and 148 hr after acid = 4.5 +/- 0.3) and microscopic evidence of minimal persistent injury. These data document the pulmonary damage and repair resulting from airway acid instillation.

Animals↗

Benzaldehyde, 2-hydroxybenzoyl hydrazone derivatives as inhibitors of the corrosion of aluminium in hydrochloric acid.

The effect of benzaldehyde, 2-hydroxybenzoyl hydrazone derivatives on the corrosion of aluminium in hydrochloric acid has been investigated using thermometric and polarization techniques. The inhibitive efficiency ranking of these compounds from both techniques was found to be: 2>3>1>4. The inhibitors acted as mixed-type inhibitors but the cathode is more polarized. The relative inhibitive efficiency of these compounds has been explained on the basis of structure of the inhibitors and their mode of interaction at the surface. Results show that these additives are adsorbed on an aluminium surface according to the Langmuir isotherm. Polarization measurements indicated that the rate of corrosion of aluminium rapidly increases with temperature over the range 30-55 degrees C both in the absence and in the presence of inhibitors. Some thermodynamic data of the adsorption process are calculated and discussed.

Aluminum↗