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At least 217 records · Page 12Linked to original sources

[Complex evaluation of the action of inhibitors of hydrochloric acid secretion on gastric function in ulcer disease].

AIM: To characterize actions of inhibitors of hydrochloric acid secretion on gastric function and to formulate indications to using different antisecretory drugs in ulcer disease (UD). MATERIAL AND METHODS: Of 120 examinees with duodenal ulcer (DU), 40 received gastrocepin, 40--famotidin, 40--omeprasol. Follow-up study was made of motor, acid-, pepsin- and mucus-forming functions of the stomach. RESULTS: By reducing production of acid and pepsin, gastrocepin is inferior to famotidin and omeprasol. Gastrocepin is more effective than famotidin and omeprasol in motor-evacuatory dysfunction. Gastrocepin improves defensive properties of gastric mucus better. CONCLUSION: The results expand indications for a differential administration of antisecretory drugs in UD.

Adult↗

Persistent asthma after inhalation of a mixture of sodium hypochlorite and hydrochloric acid.

Chlorine gas inhalation can lead to temporary mucous membrane irritation, pulmonary edema, and transient bronchospasm. Existence of respiratory sequelae is debated. We report a case of asthma, persisting 2 years after the inhalation of a mixture of sodium hypochlorite and hydrochloric acid. Bronchial histologic findings and transmission electron microscopy examinations showed uncommon abnormalities supporting irritation for cause of this nonimmunologic asthma.

Accidents, Home↗

Use of hydrochloric acid to clear obstructed central venous catheters.

Central venous catheters are being used with increasing frequency to administer drugs, and as a result, catheter obstruction caused by precipitation of poorly soluble fluid components has become a common problem. We report our first experience using 0.1 N hydrochloric acid to restore patency to central venous catheters obstructed from insolubility-induced precipitation. Precipitation was caused by drug as well as calcium and phosphorus incompatibilities. The initial use of urokinase in two cases was unsuccessful in restoring catheter patency. In all four cases, the instillation of 0.2-1.0 ml of HCl cleared the catheters. Catheter patency usually was gained immediately. No side effects were noted. Our experience supports preliminary data (JPEN 9 (suppl):255, 1985) which suggest that 0.1 N HCl is effective in clearing insolubility-induced precipitation in central venous catheters.

Acetates↗

Influence of UV rays on Feulgen-type staining with azure A-SO2 prepared with normal hydrochloric acid and sodium thiosulphate.

This communication presents a new method for the preparation of azure A-SO2 for use in Feulgen procedure. The salient feature of this method lies in the fact that azure A-SO2 can be decolourised with normal hydrochloric acid and sodium thiosulphate. The pH of this dye reagent is 2.3 and it is of water colour after filtration. The pH of this dye-reagent is raised to 4.0 with an aqueous solution of sodium hydroxide. Nuclear colouration with this newly developed dye-reagent on acid-hydrolysed DNA of tissue sections becomes fairly satisfactory under the usual laboratory conditions. Staining with this dye-reagent under exposure to UV ray is, however, vastly improved within 5 minutes as compared with the control. Stained sections do withstand treatment in SO2 water without exhibiting any leaching of the dye from the nuclei. Possible mode of action of UV rays in increasing the intensity of staining as well as the speed of reaction has been suggested.

Animals↗

Differential lung ventilation after unilateral hydrochloric acid aspiration in the dog.

Differential lung ventilation (DLV) may be necessary in the supportive care of patients with severe unilateral or asymmetrical lung disease. The best method for allocating tidal volume between the 2 lungs is unknown. Eighteen mongrel dogs were given a unilateral hydrochloric acid (HCI) aspiration injury. A computer-controlled differential lung ventilation system was used to ventilate 6 dogs with equal volumes in each lung, 6 dogs with equal end-inspiratory pressure in each lung, and 6 dogs with equal end-tidal CO2 fraction in each lung. The computer allocated volume between the 2 lungs by these 3 schemes on a breath-by-breath basis and maintained PaCO2 at 35 torr and total tidal volume at 15 ml/kg. Oxygen tension fell and pulmonary venous admixture increased after aspiration. There were no differences in gas exchange among the groups. Without PEEP, differential partitioning of tidal volume is of little consequence in differential lung ventilation of asymmetrical injuries.

Animals↗

The effect of nitroprusside on pulmonary edema, oxygen exchange, and blood flow in hydrochloric acid aspiration.

In canine pulmonary capillary leak induced by intravenous oleic acid, reducing pulmonary wedge pressure (Ppw) reduces pulmonary edema, venous admixture (Qva/Qt), and cardiac output (Qt). The authors tested the possibility that in another canine model of pulmonary capillary leak, that induced by endobronchial instillation of hydrochloric acid, nitroprusside would reduce Ppw and edema without reducing Qt or oxygen delivery (QO2). In 18 dogs, the authors measured extravascular lung water (EVLW) by thermal-dye dilution and the hemodynamic and gas exchange variables before and at intervals (1, 1.5, 3, and 5 h) after .1 N HCl bronchial infusion. By 1 h, HCl increased EVLW from 175 to 250 ml and Qva/Qt from 11 to 21%. Immediately after the 1-h measurements, the dogs were divided into three equal groups: six controls (C) were maintained with a Ppw of 12 mmHg, while plasmapheresis (P) or nitroprusside (NP) reduced Ppw to 5 mmHg for the next 4 h. EVLW continued to increase to 548 ml in C, but did not increase further in P and NP. Weights of lungs excised at 5 h confirmed that P and NP reduced edema by 50% in 4 h. In C, Qva/Qt increased, but there was no reduction in Qt or QO2. In contrast, plasmapheresis reduced Qva/Qt, Qt, and QO2. With nitroprusside, Qt and QO2 were maintained despite reduced Ppw at 1.5 and 3 h, and Qva/Qt did not decrease as in Group P. We conclude that plasmapheresis-induced reduction in Ppw reduces the pulmonary capillary leak and venous admixture following acid aspiration, but this has the potentially adverse effect of reducing cardiac output and oxygen delivery.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Duodenal gastric metaplasia, gastric anatomic-functional correlations (parietal cell mass and hydrochloric acid secretion) and Helicobacter pylori. Any differences between chronic autonomous non-specific duodenitis ("non active") and duodenal ulcer?

BACKGROUND AND METHODS: Aim of the present experience was to carry out a study on a dyspeptic population in order to verify the role of Helicobacter Pylori (HP), duodenal gastric metaplasia (GM), hydrochloric acid secretion in the genesis of chronic autonomous non-specific duodenitis (ANSD). A comparison with duodenal ulcer (DU) was effected. RESULTS: Histology showed the presence of ANSD in 24.6% of dyspeptic population. GM was present in 15.1% of ANSD, in 12.8% of dyspepsia without ANSD and in 78.1% of DU. HP in duodenum was present in 12.1% of ANSD, in 10.8% of cases of dyspepsia and in 75% of DU. Concerning parietal cell mass and acid secretion in ANSD and in dyspepsia was found a prevalence of normoparietalism with normochlorhydria, while in DU was found a prevalence of hyperparietalism with hyperchlorhydria. This study shows that the role of HP has not a well defined etiologic weight in ANSD. CONCLUSIONS: The observations of the present experience, which differentiate ANSD and DU, lead to exclude a pathogenetic relation between ANSD and DU.

Adult↗

Neutrophil proteinases in hydrochloric acid- and endotoxin-induced acute lung injury: evaluation of interstitial protease activity by in situ zymography.

We investigated the role of polymorphonuclear neutrophil (PMN) proteinases, elastase, and gelatinase B in rat models of acute lung injury. Three groups of rats were studied 6 hours after unilateral instillation of hydrochloric acid (HCl; 0.1 N), lipopolysaccharide (LPS) (4 microg), or saline. The results demonstrated that HCl-induced lung injury, as compared with LPS-induced lung injury, was associated with an increase in permeability (wet/dry weight ratio and proteins in bronchoalveolar lavage fluid). In contrast, there was similar PMN recruitment (in bronchoalveolar lavage fluid and myeloperoxidase activity in lung homogenates) and similar proteinase exocytosis (residual alveolar PMN content of elastase and gelatinase B) in both types of lung injury. In situ zymography, evaluating interstitial protease/inhibitor balance, demonstrated a decrease in gelatinolytic activity in both HCl- and LPS-injured lungs compared with normal lung. The increase in interleukin 6 concentration in lung homogenates, which is observed after both injuries compared with saline-instilled animals, could be involved in up-regulation of tissue inhibitor of matrix metalloproteinase-1, shown by immunocytochemistry to participate in antiproteinase excess. Neither inhibition of alveolar neutrophil influx using a leukocyte elastase inhibitor (EPI-hNE-4) nor inhibition of gelatinase activities by recombinant adenovirus for the human tissue inhibitor of matrix metalloproteinase 1 gene transfer decreased lung edema in HCl-induced injury. These data suggest that PMN proteinases do not contribute to HCl-induced acute lung injury in rats.

Adenoviridae↗

The rational use of i.v. hydrochloric acid in the treatment of metabolic alkalosis.

A method for the assessment and management of factors both causing and maintaining a primary metabolic alkalosis is presented. During a 2-year period 65 patients with metabolic alkalosis were treated with saline and potassium chloride infusions. In four patients the alkalosis was refractory and required additional therapy. An infusion of hydrochloric acid 0.12-0.24 mol/litre through a central venous line corrected the alkalosis without causing haemolysis or tissue necrosis. The maximum rate of infusion suggested is 0.2 mmol H+-kg body wt-1-h-1.

Aged↗

Hydrochloric acid. A trigger of cell proliferation in the esophagus of dogs.

The effect of a single instillation of acid and pepsin on the cell proliferation in the distal esophageal mucosa was investigated in four dogs. The doses of acid and pepsin used were lower than those provoking acute esophagitis and erosions. Using in vitro labeling with [3H]thymidine and autoradiography, the epithelial mitotic and DNA synthesis indices were determined at 0, 4, 8, 12, 16, 20, and 24 hr after instillation of saline, of, acid alone, or of acid with pepsin. Instillation of acid alone was followed, 16 hr later, by an increase (P less than 0.01) in DNA synthetic activity in the proliferative area. A mitotic peak (P less than 0.01) started from the 20th hour. After instillation of acid with pepsin in the same animals, a similar sequence of kinetic phenomena was observed, suggesting that the concentration of pepsin used did not potentiate the stimulating effect of acid on the cell proliferation in this epithelium. Our data indicate that hydrochloric acid stimulates the proliferative activity in the normal esophageal epithelium.

Animals↗

Intravenous hydrochloric acid in patients with metabolic alkalosis and hypercapnia.

During a seven-year period, 15 patients admitted to an intensive care unit with a metabolic alkalosis resistant to saline and potassium chloride infusions and with an arterial pH of greater than 7.44 and arterial carbon dioxide pressure (PaCO2) of greater than 50 mm Hg, while breathing spontaneously, were given hydrochloric acid at 200 mmol/24 h through a central venous line until the arterial pH had decreased to less than 7.36 or PaCO2 had decreased to less than 40 mm Hg. Five patients without respiratory failure had a significant decrease in PaCO2, pH, bicarbonate Ion (HCO3-), and base excess (BE). Four patients with acute respiratory failure had a significant decrease in PaCO2, HCO3-, and BE and an increase in arterial oxygen pressure, indicating that in both of these patient groups alveolar ventilation had improved. Six patients with chronic respiratory failure had a significant decrease in pH, HCO3-, and BE, although there was no significant change in PaCO2, indicating that in this patient group alveolar ventilation could not be consistently increased in response to a reduction in arterial pH.

Acute Disease↗