Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “HYDROCHLORIC ACID”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,765 records · Page 98Linked to original sources
PubMed1990

Intraluminal release of PGE2 due to gastric perfusion of urethane-anaesthetized rats with hydrochloric or taurocholic acid.

We have measured the intragastric release of prostaglandin E2-like immunoreactivity (PGE2-li), pH changes and mucosal damage in response to gastric perfusion with hydrochloric or taurocholic acid at pH 1.5 in urethane-anaesthetized rats. Hydrochloric acid-perfusion caused a reversible decrease in pH values, no damage to the gastric mucosa and an intraluminal release of PGE2-li. Exposure to an ulcerogenic dose (25 mM) of taurocholic acid produced an intraluminal release of PGE2-li much higher than that of the non-ulcerogenic perfusion with hydrochloric acid. These findings indicate that intraluminal release of PGE2-li, thought to play a role as an endogenous antiulcer factor, can occur in response to a stimulus producing a significant damage of the gastric mucosa or to a mild irritant stimulus.

Anesthesia↗
PubMed1997

Expression of the cyclooxygenase-2 gene in gastric epithelium.

This study examined the mRNA level of cyclooxygenase-2 (cox-2) in a rat gastric mucosal cell line after growth stimulation in vitro and in rat gastric mucosa before and after acid-induced injury in vivo. RGMI cells were stimulated with fetal calf serum in the in vitro study. Thereafter, the cox-2 mRNA level was examined by Northern analysis. Effects of NS-398, a specific inhibitor of cox-2, and indomethacin on prostaglandin production and cell proliferation were examined in RGM1 cells. In the in vivo study, rats were given 1 ml of 0.6 N hydrochloric acid into the stomach. The level of cox-2 mRNA was examined in rat gastric mucosa after acid administration. Cox-2 mRNA increased 20-60 min after growth stimulation in RGM1 cells. Both NS-398 and indomethacin suppressed prostaglandin production and cell proliferation after growth stimulation. Expression of cox-2 mRNA was observed 40 and 60 min after administration of 0.6 N HCl. Gastric lesions developed within 60 min after HCl administration and healed significantly within 48 h. The present study shows the expression of cox-2 in gastric epithelial cells in vitro and in gastric mucosa after injury in vivo. The results also suggest that cox-2 is involved in de novo synthesis of prostaglandins and cell proliferation in gastric epithelium.

Animals↗
PubMed2000

Effects of rabbit gastrointestinal mucins and dextran on hydrochloride diffusion in vitro.

We compared a viscous fingering formation of hydrochloric acid (HCl) in rabbit corpus, antral and duodenal mucins and with dextran under neutral and acidic conditions with respect to relative viscosity, molecular mass, and carbohydrate composition. The effect of desialyzation of duodenal mucin on the viscous fingering formation of HCl was also examined. HCl (0.1 N) was injected into 1% solutions of mucins and dextran and a subsequent viscous fingering formation was assessed based on an influx volume rate of HCl. A low influx volume rate indicates a high ability of the solutions to produce viscous fingers. The influx volume rate of HCl was lowest in duodenal mucin followed bl corpus mucin, antral mucin, and dextran at pH 7. The influx volume rate of HCl was inversely correlated with the relative viscosity of the solution. Maximum molecular masses were large in the order of corpus, antral, and duodenal mucins, and they were larger than dextran T2000. Rabbit gastrointestinal mucins were very polydisperse system. Duodenal mucin contains more sialic acid than gastric mucins; the influx volume rate of HCl increased in desialylated duodenal mucin. It is suggested that the higher ability of gastric mucins to prevent HCl diffusion than dextran were due to the differences in the molecular mass. The ability of duodenal mucin to prevent HCl diffusion was probably attributed to its high sialic acid content, which may reflect a physiological role of duodenal mucin in the duodenum that has to deal with HCl influx from the stomach.

Animals↗
PubMed1996

The acute impact of NaHCO3 in treatment of metabolic acidosis on back-titration of non-bicarbonate buffers: a quantitative analysis.

OBJECTIVE: The major non-bicarbonate buffers are intracellular proteins, a detrimental effect of severe acidosis could be their titration with H+. This in turn would lead to their net charge becoming more positive, and possibly, to changes in their shape and function. Since NaHCO3 is a treatment option in patients with severe metabolic acidosis, the purpose of this study was to examine the acute effect of the administration of NaHCO3 on back-titration of non-bicarbonate buffers in metabolic acidosis. DESIGN: Prospective, controlled, non-randomized laboratory study. SETTING: Research laboratory. SUBJECTS: 21 male Wistar rats. INTERVENTION: Rats were anesthetized, intubated and ventilated. Ventilation was adjusted at the beginning of the experiment to a PCO2 of approximately 30 mmHg, no further adjustments were made thereafter. Acute metabolic acidosis was induced by the infusion of 3.5 mmol of hydrochloric acid over 1 hour. After an equilibration period, 3 groups of seven rats were studied; group I received 0.75 mmol NaHCO3, group II received equimolar NaCl, and group III served as time control. MEASUREMENTS AND MAIN RESULTS: Measurements were made to enable quantitation of how much HCO3 was retained in the ECF and how much was titrated with H+ and was excreted as "acid-base" CO2. Since there are so few H+ present in the ECF in a free or a bound form, and in the absence of an increase in endogenous acid-production, the source of this H+ is from proteins in the ICF. As compared to the NaCl and the time control groups, the administration of NaHCO3 led to significant alkalinization of the ECF, pH rose from 7.22 +/- 0.03 to 7.34 +/- 0.02. Of the 0.75 mmol of NaHCO3 that was administered, 67% or 0.52 +/- 0.08 mmol was retained in ECF. Only a small amount (0.07 +/- 0.09 mmol) of acid-base CO2 was excreted. CONCLUSIONS: The administration of NaHCO3 does not acutely lead to a significant back-titration of non-bicarbonate buffers, especially under conditions of fixed ventilation.

Acidosis↗
PubMed1969

Taste nerve fibers: a random distribution of sensitivities to four tastes.

The numbers of rat glossopharyngeal and chorda tympani fibers responding to one, two, three, or four taste stimuli of different quality (sodium chloride, hydrochloric acid, quinine, and sucrose) and to each of the six possible pairs of these stimuli can be predicted if there are four independent sensitivities randomly distributed among innervating fibers.

Animals↗
PubMed1995

Matrix effects in the determination of zinc(II) ion in whole rat liver by flame atomic absorption spectrometry.

Analytical systems that might be of practical importance for the direct determination of ZnII ion in whole rat liver homogenates by flame atomic absorption spectrometry were reliably evaluated based on the change in calibration sensitivity. For that purpose synthetic samples were prepared in three extremely different media for tissue homogenization. Hydrochloric acid medium proved to be more resistant to matrix components (non-ionic detergent, albumin, inorganic salts) than water or Tris-acetate buffer (pH 8.7). Further, a highly acidic medium allows the substitution of complex albumin and salt-containing standard solution with simple acidic and even aqueous solutions. The convenience of 1.0 mol l-1 HCl as the medium for rat liver homogenization is emphasized, owing not only to quantitative extraction of metal ions but also to markedly reduced matrix effects.

Acetates↗
PubMed1984

[Preparation and transplantation of demineralized bone tissue].

The use of demineralized bone transplants is found to increase the effectiveness of allogenic transplantations of bone tissue due to its ability to induce active osteogenesis even when implanted intramuscularly. The method of preparing the bone transplants by demineralization in solutions of hydrochloric acid should be widely used in traumatology and orthopedy.

Adolescent↗
PubMed1984

Hyperchloremic metabolic acidosis after chlorine inhalation.

Chlorine gas inhalation is usually accompanied by pulmonary toxicity and hypoxemia; the associated acidemia, when present, has been attributed to lactic acidosis. This case report describes the development of hyperchloremic metabolic acidosis following accidental chlorine gas exposure. The mechanism postulated for the production of this acidosis is the absorption of hydrochloric acid following the reaction of chlorine gas with tissue water. This may be the first case of chlorine toxicity in which the mechanism of the acidosis has been determined.

Accidents, Home↗
PubMed1990

CD18-dependent and -independent mechanisms of neutrophil emigration in the pulmonary and systemic microcirculation of rabbits.

Neutrophil (PMN) migration in the systemic and pulmonary circulation of rabbits was compared by using different inflammatory stimuli to determine the role of the leukocyte adhesion complex, CD11/CD18, in each of these vascular beds. The adhesion complex was blocked by administering the anti-CD18 mAb 60.3. The data show that mAb 60.3 blocks PMN emigration into inflammatory foci in the abdominal wall produced by implanting sponges containing either hydrochloric acid, Streptococcus pneumoniae, Escherichia coli endotoxin, or PMA. mAb 60.3 also inhibited PMN emigration in response to peritoneal instillation of S. pneumoniae. The effect of mAb 60.3 on PMN emigration in the lungs varied depending upon the stimulus. PMN failed to migrate into the PMA-induced pneumonia; however, mAb 60.3 pretreatment only partially inhibited endotoxin-induced pneumonia and did not inhibit S. pneumoniae or hydrochloric acid-induced pneumonias. PMN lavaged from the alveolar spaces in the Streptococcal pneumonia had similar quantities of mAb 60.3 bound to their surfaces as the circulating PMN. We conclude that the CD11/CD18 complex mediates PMN adherence in the systemic circulation. However, PMN adherence in the pulmonary circulation may occur by either CD18-dependent or -independent mechanisms that are specific to the inciting stimulus.

Animals↗
PubMed2006

Protective effect of the in situ pellicle on dentin erosion - an ex vivo pilot study.

AIM: The acquired pellicle is well known as an anti-erosive proteinaceous layer on enamel, but its protective properties on dentin have not been investigated in detail until now. The aim of the present ex vivo study was to evaluate the erosive effects on pellicle coated dentin. METHODS: Bovine dentin slabs were exposed to the oral cavity of one subject for 120 min for in situ pellicle formation. Subsequently, the slabs were incubated with HCl (pH 2.3) in vitro for 5 min and erosive calcium-release was measured photometrically. In addition, the acid treated specimens were evaluated by transmission electron microscopy (TEM). Pellicle free samples served as controls. RESULTS: Calcium erosion from the pellicle coated dentin slabs amounted to 23.5+/-2.9 microg Ca/min (pellicle free samples: 32.2+/-4.2 microg Ca/min). The difference was statistically significant (p < or = 0.05). In pellicle coated as well as in uncoated dentin samples, TEM-evaluation showed a demineralised dentinal surface layer which thickness ranged between 3 and 6 microm. The pellicle itself was partially dissolved but not removed by hydrochloric acid treatment. CONCLUSION: The protective properties of the acquired pellicle against an erosive challenge of the dentinal surface are limited. The dentinal pellicle functions like an ion permeable network rather than a barrier.

Adult↗
PubMed1982

Respiratory illness caused by overheating of polyvinyl chloride.

On 9 August 1979, 62 (30.8%) of 201 workers and one of 60 management personnel in a polyvinyl chloride (PVC) fabricating plant developed acute upper and lower respiratory irritation, headache, nausea, and fainting. All were taken to hospital; none died. Sixty of the patients were women. Interviews two weeks later with 57 affected and 14 unaffected workers disclosed that illness had followed exposure to fumes from an overheated (362 degrees C) PVC extruding machine. Fumes were emitted from 1100 until 1150; cases occurred from 1100 until late afternoon. All workers who became ill worked west of the overheated extruder, and the affected manager had visited that area. The earliest cases occurred closest to the machine, and incidence decreased (from 53.3% to 15.4%) with distance westward. This pattern was consistent with plant ventilation. Incidence rates in men and women did not differ (p greater than 0.1). At two and 14 weeks, pulmonary function testing of workers with persistent pulmonary symptoms showed abnormalities in 13 of 16 and in 9 of 11 respectively; the group with persistent symptoms contained an excess of non-smokers and of those with previous respiratory illnesses. One kilogram of PVC heated to 300 degrees C releases an estimated 12.9 g of hydrochloric acid (HCl) and 4.9 g of carbon monoxide (CO). We attributed the outbreak to exposure to toxic HCl and CO and rejected the hypothesis of mass psychogenic illness.

Carbon Monoxide Poisoning↗
PubMed1996

Does the administration of carbicarb lead acutely to back-titration of non-bicarbonate buffers?

OBJECTIVE: We have recently demonstrated in a model of acute metabolic acidosis in rats that the administration of NaHCO3 does not lead acutely to back-titration of non-bicarbonate buffers. Carbicarb is a new alkalinizing agent that has been proposed as a replacement for NaHCO3 in the treatment of metabolic acidosis. Hence, the purpose of this study was to examine the impact of carbicarb on back-titration of non-bicarbonate buffers. METHODS: Rats were anaesthetized, intubated and ventilated to a PCO2 of approximately 30 mmHg. Acute metabolic acidosis was induced by the infusion over 1 hour of 3.5 mmol of hydrochloric acid. After a 20 min equilibration period, 3 groups of rats (n = 7 in each group) were examined. Rats in groups I received 0.75 meq of Na from 1 M carbicarb solution as an intravenous bolus, rats in group II received equimolar NaCl, while rats in group III were used as time controls. Calculations were performed to quantitate the amount of HCO3- that was retained in the ECF volume and the amount that was titrated with H+ and excreted as "acid-base" CO2. "Acid-base" CO2 was considered as the amount of CO2 that was excreted in excess of what would be produced during metabolism. RESULTS: As compared to the NaCl and the time control groups, the administration of carbicarb led to significant alkalinization of the ECF, pH rose from 7.23 +/- 0.02 to 7.34 +/- 0.03. Of the 0.75 mmol of carbicarb that was administered, 0.61 +/- 0.05 mmol (70%) was retained in ECF. There was virtually no "acid-base" CO2 produced. CONCLUSIONS: The administration of carbicarb does not lead acutely to back-titration of non-bicarbonate buffers especially under conditions of fixed ventilation.

Acidosis↗
PubMed1985

Duodenal acidification releases cholecystokinin.

We studied the effect of hydrochloric acid (HCl) in the proximal small intestine on release of cholecystokinin (CCK) and secretin and on exocrine pancreatic secretion in conscious dogs with gastric cannulas and modified Herrera pancreatic cannulas. Intraduodenal administration of HCl in a concentration of 50 or 100 mM at rates of 0.05, 0.1, 0.2, and 0.4 mmol/min significantly increased plasma concentration of CCK in a dose-dependent manner, whereas plasma gastrin levels decreased. The increased plasma CCK level paralleled a significant increase in pancreatic trypsin output. Plasma secretin concentration and pancreatic bicarbonate output also increased in response to the acid, and the increase was dependent on the acid loads delivered in the duodenum. Thus, in dogs, HCl in the duodenum releases both CCK and secretin to stimulate pancreatic secretion of bicarbonate as well as enzymes.

Animals↗
PubMed2004

[Validation of a method for discrimination of formaldehyde processing in textile products].

It is important to investigate a cause of formaldehyde contamination exceeding a regulation limit value in a textile product. If formaldehyde was released from a textile product itself by treatment or processing with formaldehyde, an administrative guidance is given to a manufacture. On the other hand, when the formaldehyde migrated from other textile products or a furniture stand during displaying, an improvement instruction is performed to the store. Iwama et al. [Ann. Rep. Nagoya City Public Res. Inst., 42, 11-16 (1996)] developed a method for distinguishing fabric processing and migration by additional hydrolytic extraction using hydrochloric acid solution. This study was to confirm the reliability and stability of the method for knowing formaldehyde processing on textiles. Five laboratories evaluated three samples: unprocessed textile, processed textile and unprocessed but formaldehyde-migrated textile. For a processed textile sample, amounts of formaldehyde increased by additional extractions with acidic solution, so all laboratories judged that the sample had been treated with formaldehyde. In the cases of the other two samples, such increases were not observed in the extracts using acidic solution. All laboratories reported that these samples were not processed using formaldehyde but had absorbed a different level of formaldehyde by migration. In a series of experiments, the judgement about the existence of formaldehyde processing or migration is comparatively consistent among all laboratories. This validation study concluded that the distinguishing method adopting additional extractions with acidic solution is useful to find formaldehyde processing of textile, and to deal with processing and migration separately as a cause of formaldehyde contamination.

Consumer Product Safety↗
PubMed1983

Aspiration pneumonia: treatment with pulmonary vasodilators.

Experimental aspiration pneumonia induced in the isolated perfused ventilated canine pulmonary lobe by the intrabronchial instillation of hydrochloric acid is characterized by pulmonary edema, intrapulmonary shunting, and loss of lung compliance. In addition, pulmonary artery pressure increases. In an attempt to modify the injury response, we restricted the increase in pulmonary artery pressure in the isolated lobe model by administering vasodilator drugs. In control lobes perfused for 4 hours there was minimal weight gain (14 gm), pulmonary artery pressure remained stable (13 mm Hg), and intrapulmonary shunting did not occur. Following intrabronchial instillation of 0.2 ml of 0.1N HCl/gm of lobe weight, lobe weight tripled (183 gm), pulmonary artery pressure (20 mm Hg) was significantly increased, and significant intrapulmonary shunting (32%) developed. When sodium nitroprusside (2 micrograms/min/kg of dog body weight) was infused into the pulmonary artery 3 minutes after HCl instillation, the pulmonary artery pressure was significantly reduced (13 mm Hg) compared to that in untreated acid lobes. This was accompanied by a significant reduction in mean weight gain (100 gm) and intrapulmonary shunting (15%) compared to untreated acid lobes. Similarly, when isoproterenol (0.04 micrograms/min/kg dog body weight) was infused into the pulmonary artery following acid instillation, the pulmonary artery pressure (12.5 mm Hg) was significantly reduced compared to that in untreated acid lobes. This was also accompanied by a significant reduction in weight gain (60 gm) and intrapulmonary shunting (6%) compared to untreated acid lobes. These data demonstrate that the increase in pulmonary artery pressure following acid injury can be lowered pharmacologically and that a significant decrease in injury response follows. This suggests that the magnitude of the injury response is in part a function of pulmonary artery pressure.

Animals↗
PubMed1981

Retroperistaltism and duodenogastric reflux in dogs.

Motility of the antrum, pyloric sphincter, duodenal bulb and proximal duodenum was recorded in unanesthetized dogs. Retroperistaltism and reflux of intestinal contents were regularly produced by apomorphine and occurred often with or without vomiting when large amounts of hydrochloric acid were infused or delivered into the small intestine. Retroperistaltism was found occasionally after intravenous infusion of adrenalin, carbachol or pentagastrin. Reverse peristalsis was characterized by strong and long lasting contractions of the duodenum migrating orad.

Animals↗