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PubMed2003

Complete degradation of perchlorate in ferric chloride and hydrochloric acid under controlled temperature and pressure.

Despite favorable thermodynamics, the reduction of perchlorate (ClO4-) is kinetically limited in aqueous media because of its high activation energy. In this paper, a new methodology has been presented for degrading ClO4- in an FeCl3-HCl solution at an elevated temperature (< 200 degrees C) and/or pressure (approximately 20 atm). Results indicate that the rate constant for the pseudo-first-order reaction between ClO4- and ferrous Fe(II) (in excess) increased nearly 3 orders of magnitude when the temperature was increased from 110 to 195 degrees C, and a complete reduction of ClO4- occurred in < 1 h at 195 degrees C in the FeCl3-HCl solution. The activation energy of the reaction was calculated to be about 120 kJ/mol. Additionally, a flow-through reactor was constructed based on the batch kinetic measurements, and a nearly complete degradation of ClO4- was observed under continuous-flow mode. Because the FeCl3-HCl solution has been successfully used in regenerating selective anion-exchange resins sorbed with ClO4- during water treatment, this new methodology offers a cost-effective means to degrade ClO4- while not altering the chemical properties of the FeCl3-HCl regenerant solution so it can be reused, eliminating the production of secondary wastes.

Anion Exchange Resins↗
PubMed2001

Activation of alveolar phospholipase A2 after hydrochloric acid aspiration in rats.

PURPOSE: The present study was carried out to determine phospholipase A2 (PLA2) activity in the bronchoalveolar lavage fluid (BALF) in rats subjected to HCI aspiration. MATERIALS AND METHODS: Rats were allocated into one of five groups. Groups H-1 and H-3 received instillation of HCI into lungs. Groups S-1 and S-3 received saline instead of HCI. Group C received no instillation. BAL was performed according to the protocol, that is, 1 hour after the instillation in groups H-1 and S-1, 3 hours after the instillation in groups H-3 and S-3, and arbitrarily in group C. Obtain BALF was analyzed for the protein concentration, PLA2 activity, and the molecular mass of PLA2. RESULTS: The protein concentration in BALF showed an increase in groups H-1 and H-3. PLA2 activity decreased in group H-1, but increased in group H-3, compared with groups S-1 and S-3, respectively. PLA2 in groups C and H-1 revealed a high molecular mass (HM), but that in group H-3 revealed a low molecular mass (LM). CONCLUSIONS: There is an increase in the alveolar LM-PLA2 at inflammatory phase after HCI aspiration, suggesting the pathophysiologic role of LM-PLA2 in the acute lung injury.

Animals↗
PubMed1983

Lung mechanics following aspiration of 0.1 N hydrochloric acid.

Pressure-volume curves were obtained from excised left lungs of goats at 4, 24, and 48 h after tracheal instillation of 2.5 ml/kg of 0.1 N HCl. Air total lung capacity (TLC) at transpulmonary pressure (PL) = 35 cmH2O was 38.8 ml/kg body weight before acid, and was reduced sharply to 21.1 at 4 h, then increased to 25.6 at 24 h and 32.1 at 48 h. Excess extravascular lung water (EVLW) could account for only part of the volume reductions. Specific compliance ratio of transpulmonary pressure to total lung capacity (CL/TLC) between PL of 5 and 0 cmH2O was reduced from 0.074/cmH2O to 0.050, 0.048, and 0.053/cmH2O, respectively. Saline TLC (PL = 10 cmH2O) changed from 44.8 to 32.4, 34.3, and 45.4 ml/kg, respectively, but CL/TLC did not, suggesting airway obstruction. After injury, trapped volume at PL = 0 increased from 24.9 to 29.2, 43.3, and 37.3% TLC with air, and from 20.3 to 38.5, 33.1, and 28.5%, respectively, with saline. Air volume at a PL = 10 cmH2O on deflation fell from 82.0 to 72.1% TLC at 4 h, but was near control at 24 and 48 h. The reduction in ventilated volume was not reflected in proportionately increased shunt; therefore, some compensatory vasoconstriction must have occurred. We suggest that in affected regions increased surface forces, increased EVLW, and airway obstruction caused reductions of lung volume.

Animals↗
PubMed1988

Perfusion distribution and lung thermal volume in canine hydrochloric acid aspiration.

We investigated the effects of a brief period of positive end-expiratory pressure (PEEP) ventilation or nitroglycerin (NTG) infusion on the distribution of pulmonary blood flow and extravascular thermal volume (ETV) in anesthetized dogs with unilateral HCl lung injury. ETV was determined by the thermal dye technique by use of a monoexponential extrapolation to exclude recirculating indicator, and regional blood flow was determined by a particle distribution technique (radiolabeled plastic microspheres). The lungs were weighted after the animals were killed, and extravascular lung mass (ELM) was determined with the use of hemoglobin to correct for trapped lung blood. Measurements were obtained before instillation of HCl into the right lung and repeated 3 h later before, during, and after PEEP ventilation or NTG infusion. Fractional perfusion of the severely injured portion of the right lung (Qinj/QT) fell from 44.3 +/- 11.1% at base line to 27.8 +/- 15.4% after the onset of lung injury. PEEP produced an acute reversible increase in ETV (63 +/- 37% over average of pre- and post-PEEP values), and the changes in ETV were closely correlated with changes in Qinj/QT (r = 0.91). NTG infusion produced insignificant increases in ETV (14 +/- 10% over average of pre- and postinfusion values) and Qinj/QT (59 +/- 35%), but the changes in ETV and Qinj/QT were strongly correlated (r = 0.92). The fraction of extravascular lung mass detected by the thermodilution measurement averaged 0.44 (range 0.24-0.77).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2004

Effects from pretreatment of stannous fluoride versus sodium fluoride on enamel exposed to 0.1 M or 0.01 M hydrochloric acid.

Preventing enamel erosions caused by acidic soft drinks or from vomiting during eating disorders is a challenge in current dental research. The aim of this study was to examine whether pretreatment of dental enamel with a solution of 0.4% SnF2 could prevent dissolution of human enamel exposed to solutions of 0.1 M HCl, pH 1.2 or 0.01 M HCl at pH 2.2. Human enamel was pretreated for 18 h with a solution of 0.4% SnF2 and with control solutions of 2% NaF or distilled water, and then exposed to HCl solutions. Similar experiments were performed with teeth treated for 2 min SnF2 and then 4 min HCl. The effect was monitored by scanning electron microscopy (SEM) and by chemical analysis. At pH 2.2, NaF and water treatments showed minor inhibition of enamel dissolution, whereas SnF2 inhibited demineralization significantly also after 2 min pretreatment and 4 min HCl exposure. At pH 1.2, SEM showed severe dissolution of the enamel surfaces regardless of pretreatment. As pH of stomach vomit is usually > 1.5, SnF2 may be an interesting agent for use in the treatment and prevention of dental erosions even in patients with frequent vomiting episodes.

Bicuspid↗
PubMed2002

Histamine release by hydrochloric acid is mediated via reactive oxygen species generation and phospholipase D in RBL-2H3 mast cells.

In order to investigate the underlying mechanism of HCl in oesophagitis, the inflammatory response to HCl was observed in RBL-2H3 mast cells. Rat basophilic leukemia (RBL-2H3) cells were used to measure histamine release, arachidonic acid (AA) release, reactive oxygen species (ROS) and peroxynitrite generation induced by HCl. Exogenous HCl increased the level of histamine release and ROS generation in a dose dependent manner, whereas it decreased the spontaneous release of [3H] AA and the spontaneous production of peroxynitrite. Mepacrine (10 microM), oleyloxyethyl phosphorylcholine (10 microM) and bromoenol lactone (10 microM) did not affect both the level of histamine release and ROS generation induced by HCl. U73122 (1 microM), a specific phospholipase C (PLC) inhibitor did not have any influence on level of histamine release and ROS generation. Propranolol (200 microM), a phospholipase D (PLD) inhibitor, and neomycin (1 mM), a nonspecific PLC and PLD inhibitor, significantly inhibited both histamine release and ROS generation. Diphenyleneiodonium (10 microM), a NADPH oxidase inhibitor, and tiron (5 mM), an intracellular ROS scavenger significantly inhibited the HCl-induced histamine release and ROS generation. These findings suggest that the inflammatory responses to HCl is related to histamine release and ROS generation, and that the ROS generation by HCl may be involved in histamine release via the PLD pathway in RBL-2H3 cells.

Animals↗
PubMedDate not supplied

[Electromanometry of the upper esophageal sphincter before and after esophageal perfusion with hydrochloric acid 0,1N. Experimental study in dog].

BACKGROUND: The responses of the upper esophageal sphincter to gastroesophageal reflux is controversial. OBJECTIVE: Study the effect of upper esophageal sphincter to the esophageal acid perfusion. METHODS: Thirty adult dogs of both sexes were studied, being submitted to esophageal electromanometry. The pull through technique and continuous infusion of the catheters with distilled water were employed. These exams allowed us to measure the pressure width (mm Hg) and the length (cm) of the upper esophageal sphincter in basal conditions (moment 1). After this first phase the animals were submitted to esophagic infusion, being then divided in three groups, according to the solution used in the infusion and the moment of the study, as follows: Group 1: esophagic infusion with distilled water and electromanometric studies accomplished 15 minutes (moment 2) and 30 minutes (moment 3) of the end of the infusion. Group 2: esophagic infusion with HCl 0.1 N and electromanometric studies accomplished 15 minutes after the end of the infusion (moment 2). Group 3: esophagic infusion with HCl 0.1 N and electromanometric studies accomplished 30 minutes after the end of the infusion (moment 3). RESULTS/CONCLUSIONS: This research was performed to evaluate the esophagic acidification influence on the upper esophageal sphincter. The observed results allowed us to conclude that the acidification of the esophagus did not cause any alteration on the pressure width and on the length of the upper esophageal sphincter.

Animals↗
PubMed1992

Blood pressure and gastric motor responses to bradykinin and hydrochloric acid injected into somatic or visceral tissues.

Both visceral and somatic nociceptive stimuli elicit reflex changes in blood pressure and gastric motor activity, but the exact type of response varies with the type of nociceptive stimulus and its site of application. Therefore, the present study compared the effects of visceral (i.p. or i.a.) and somatic (s.c.) administration of bradykinin and HCl on both mean arterial blood pressure (MAP) and intragastric pressure in anaesthetized rats. The nervous pathways mediating these responses were investigated by surgical or pharmacological inhibition of the possible reflex arcs. Bradykinin (i.a.--into the aortic arch, i.p., and s.c.), and HCl (i.p. and s.c.), elicited a fall in MAP followed by a transient increase. Intragastric pressure decreased in response to administration of these chemicals. Acute coeliac ganglionectomy reduced the gastric relaxations in response to both bradykinin and HCl, whereas vagotomy reduced only the gastric relaxations induced by HCl. Neither lesion influenced the changes in MAP after either chemical. Ablation of small diameter afferents by capsaicin or chemical sympathectomy by guanethidine reduced the changes in MAP after both chemicals, except that which occurred after i.a. injection of bradykinin. The secondary increase in MAP after i.a. and i.p. administration of algesics was increased after guanethidine. Both pretreatments reduced gastric relaxations in response to either chemical. Pretreatment of the rats with the bradykinin antagonist Hoe-140 reduced the responses to bradykinin but not to HCl. The results show that both visceral and somatic administration of painful chemicals elicit reflex falls in MAP and intragastric pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Human duodenal mucosal bicarbonate secretion. Evidence for basal secretion and stimulation by hydrochloric acid and a synthetic prostaglandin E1 analogue.

The factors responsible for prevention of duodenal mucosal injury are not known. This series of experiments was performed to determine whether the human duodenum secretes bicarbonate that could prevent mucosal damage. To isolate a 4-cm segment of proximal (i.e., the duodenal bulb) or distal duodenum free of contamination from either gastric or pancreaticobiliary secretion, or both, methods were developed using occlusive balloons. The test segment was perfused with NaCl (2 ml/min, 37 degrees C) containing [14C]PEG as a nonabsorbable marker, and bicarbonate output was quantitated. Mean (+/- SE) basal proximal duodenal bicarbonate output was 143 +/- 17 mumol/cm X h. A 5-min infusion of 25, 50, and 100 mM HCl directly into the isolated proximal duodenal test segment increased bicarbonate output to 167 +/- 29, 199 +/- 19, and 278 +/- 49 mumol/cm X h, respectively, during the hour after acidification. Distal duodenal acidification (25, 50, and 100 mM) also increased bicarbonate output from the isolated proximal duodenal test segment. A synthetic prostaglandin E1 analogue, misoprostol (1.67-13.3 micrograms/min), infused directly into proximal or distal test segments significantly stimulated bicarbonate outbreak; peak responses were 644 +/- 35 mumol/cm X h and 171 +/- 20 mumol/cm X h (p less than 0.001), respectively. Thus, in humans, the proximal and distal duodenal mucosa secretes bicarbonate at rest; direct acidification of the proximal duodenum stimulates bicarbonate output; acidification of the distal duodenum beyond the isolated test segment also increased proximal duodenal bicarbonate output; and a synthetic prostaglandin E1 analogue stimulated both proximal and distal bicarbonate output; however, distal duodenal bicarbonate output was significantly less, indicating a proximal-to-distal gradient in bicarbonate secretion.

Adult↗
PubMed2003

Hydrochloric acid induced changes in macrophage migration inhibitory factor in the bladder, peripheral and central nervous system of the rat.

PURPOSE: We established the presence of the proinflammatory cytokine macrophage migration inhibitory factor (MIF) in the bladder and in nervous system structures innervating the bladder, and evaluated changes in MIF and cyclooxygenase-2 (COX-2) protein levels and expression following chemical cystitis. MATERIALS AND METHODS: Male Sprague-Dawley rats were anesthetized and a catheter was introduced into the bladder dome. Cystitis was induced by infusing 0.4 N HCl into the bladder. Control rats received a similar volume of saline. Two hours later the bladder, major pelvic ganglia (MPG), L6/S1 dorsal root ganglia (DRG) and L6/S1 spinal cord were removed and assayed for MIF and COX-2 protein, and mRNA using Western blot and quantitative reverse transcriptase-polymerase chain reaction techniques. RESULTS: Immunohistochemistry showed MIF located mainly in the urothelium of saline treated rats. Instillation of HCl into the bladder resulted in marked epithelial denudation, moderate edema and vasodilatation in the submucosa. MIF protein levels decreased but MIF mRNA expression remained unchanged in bladders treated with HCl compared with controls. However, MIF protein and mRNA levels increased in the MPG, L6/S1 DRG and L6/S1 spinal cord of HCl treated animals. COX-2 protein was not detected in the bladder, DRG or MPG of saline-treated rats. However, a small amount was present in the L6/S1 cord. On the other hand, HCl treated rats showed marked increases in COX-2 protein levels in all tissues examined. Similarly although cox-2 mRNA was constitutively expressed in all tissues examined, expression increased following HCl treatment. CONCLUSIONS: Chemical cystitis induced by intravesical HCl in rats increases the protein levels and mRNA expression of MIF and COX-2 in central and peripheral nervous system tissues that are involved in innervating the bladder. This finding suggests that MIF may be involved in bladder inflammation and may have a role in the peripheral and central nervous system pathways that regulate bladder reflexes in response to bladder inflammation.

Animals↗
PubMed1996

Effect of supplemental sodium chloride, sodium phosphate, or hydrochloric acid in starter pig diets containing dried whey.

Three experiments involving a total of 606 pigs weaned at 23 +/- 2 d of age were used to evaluate the effects of added dietary Na or Cl or both in combination (NaCl) on postweaning performance responses. A basal diet without added NaCl was formulated to 1.20% lysine using a corn-soybean protein mixture with 20% dried whey (C-SBP-DW) and was used in all experiments. The analyzed content of the basal diet for the three experiments averaged .19% Na, .37% Cl, and 1.37% K. In Exp. 1, NaCl was added to treatment diets at 0, .20, .40, and .60% at the expense of corn. The experiment was a randomized complete block (RCB) design conducted in 14 replicates using a total of 336 pigs (six pigs/ pen). The results demonstrated a linear (P < .01) growth response during the 0- to 7-d and a quadratic (P < .08) response during the 8- to 14-d period. Gain: feed ratio improved quadratically (P < .08) for the 0- to 14-d period. In Exp. 2, Na2HPO4 added to the C-SBP-DW basal diet provided supplemental Na levels of 0, .08, .16, and .24% Na to four treatment diets. The experiment was conducted in six replicates in a RCB design using a total of 144 pigs (six pigs/pen). The results demonstrated a linear (P < .05) growth response during the 0- to 7-d period as Na level increased, but not thereafter, and an improved gain: feed ratio (P < .05) for the 0- to 14-d period. In Exp. 3, Cl was added as HCl at 0, .05, or .10% Cl to the basal C-SBP-DW diet. The experiment was a RCB design conducted in six replicates using a total of 126 pigs (five or six pigs/pen between replicates). The results demonstrated a linear growth (P < .01) and feed intake (P < .08) response during the 0- to 7-d and the 0- to 14-d period to increasing levels of Cl. Feed intake also increased for the 0- to 7-d (P < .08), and 8- to 14-d (P < .05) periods. Stool looseness was unaffected by any of the dietary variables in the three experiments. These results suggest that the NRC (1988) recommendations for Na and Cl for young pigs (< or = 10 kg BW) may need to be increased.

Animal Feed↗
PubMed1999

Effect of supplemental sodium chloride and hydrochloric acid added to initial starter diets containing spray-dried blood plasma and lactose on resulting performance and nitrogen digestibility of 3-week-old weaned pigs.

Four experiments evaluated the efficacy of Na or Cl or their combination added to weanling pig diets that contained plasma protein and lactose on pig performance and N digestibility. The four experiments used a total of 563 crossbred pigs weaned at 22+/-1 d of age averaging 6.4 kg body weight. The basal diet in each experiment contained 5.8% plasma protein and 20% lactose and analyzed .20% Na and .23% Cl. In Exp. 1, NaCl was added to treatment diets at 0, .20, .40, or .60%. The trial was conducted for a 21 d period in a randomized complete block (RCB) design in seven replicates. Improved growth rates (P < .01) and gain:feed ratios (P < .01) occurred up to a dietary salt level of .40%. In Exp. 2, we evaluated the interaction of Na and Cl on pig performance. The experiment was a 2 x 2 factorial arrangement in a RCB design conducted in seven replicates. Total dietary Na was .20 or .36%, and Cl was included at .25 or .45%. Although there was a numerical increase in pig gains with added Na, the response was not significant (P > .15), but both gains (P < .01) and gain:feed ratios (P < .01) increased at the higher dietary Cl level. In Exp. 3, we evaluated the effect of five dietary levels of Cl added at .06% increments to a basal diet that analyzed .34% Na and .20% Cl on postweaning pig performance. The experiment was a RCB design conducted in eight replicates. A growth response (P < .01) to the .38% Cl level occurred during the initial 14-d postweaning period and to the .32% Cl level from 14 to 21 d. Gain:feed ratio increased each week with added Cl, but it was significant only for the period from d 0 to 7 d (P < .01). A N digestibility trial, using the diets of Exp. 3, constituted Exp. 4, and groups of three pigs per stainless steel metabolism crate were pair-fed to pigs fed the basal diet. The experiment was a RCB design conducted in three replicates over a 3-wk period. The results demonstrated a weekly decrease in fecal N (P < .01), no effect on urinary N (P < .15), improved N retention (P < .01), and an improved apparent N digestibility (P < .01) to the .38% dietary Cl concentration during the initial 2 wk postweaning. These experiments suggest that although plasma protein contributed Na and Cl to the initial diets of weaned pigs, additional Na and Cl, but particularly Cl, improved pig growth, N retention, and N digestibility. The results suggest a dietary minimum of .38% total Cl level during the initial 2 wk postweaning.

Animal Feed↗
PubMed2004

Removal of metals from industrial sludge by extraction with different acids.

This study addresses the feasibility of removing Cu and Ni from sludges of printed circuit board (PCB) plants by acidic extraction. Citric acid, acetic acid, hydrochloric acid, nitric acid, and sulfuric acid at various concentrations were experimentally examined to determine preferred conditions for removing Cu and Ni. Experimental results indicate that the removal ratios of Cu were 57% (citric acid), 79% (acetic acid), 81% (hydrochloric acid), 91% (nitric acid), and 92% (sulfuric acid), and that of Ni was 74% (citric acid), 70% (acetic acid), 75% (hydrochloric acid), 92% (nitric acid), and 93% (sulfuric acid), using 1 N extractants. The removal ratios obtained using sulfuric acid or nitric acid at a particular concentration were in the order Pb> Ni> Cu> Zn. The kinetic extraction results revealed that the extraction of Cu and Ni by nitric acid and sulfuric acid exhibited a lagphase after 60min and the removal ratio was then around 90%. The kinetic results also revealed that the extraction rate constants of Cu and Ni increased with the concentration of the acid. The extraction rate constants of Cu and Ni followed the order sulfuric acid > nitric acid > acetic acid, and it also showed that Ni was more easily extracted than Cu from PCB sludge. The total percentages of Cu extracted by 1 N acetic acid, nitric acid, and sulfuric acid, determined in three replicate extractions were 78, 94, and 94%, and those of Ni were 89, 94, and 98%, respectively. The residue sludge, following three replicate extractions using 1 N acetic acid, nitric acid, and sulfuric acid, was further tested by toxicity characteristic leaching procedures (TCLP), and more than 15 mg/L of Cu was leached, exceeding the legal concentration in Taiwan. This observation reveals that the residue sludge following three replicate extractions by acids remained hazardous waste. Further treatment, such as solidification, must be performed before the sludge is disposed of.

Acids↗
PubMed1999

Study of the Dissolution of the Barium Sulfate (001) Surface with Hydrochloric Acid by Atomic Force Microscopy.

Noncontact atomic force microscopy (NC-AFM) has been used to investigate the morphological changes of a freshly cleaved (001) surface of barium sulfate (barite) etched with an aqueous solution of 0.1 M HCl at room temperature. Shallow triangular etch pits with a height of 3.6 Å were developed in atomically flat (001) terraces. The etching of the surface was found to proceed in a layer-by-layer dissolution process. Because the crystal structure of barite exhibits a two-fold screw axis parallel to the c axis, "alternating" etch pits were formed, with any two consecutive etch pits pointing opposite to each other. These etch pits became deeper and more elongated along the b axis with time. Copyright 1999 Academic Press.

Journal Article↗
PubMed1976

Integration of biochemical functions of different cells of rat gastric mucosa for hydrochloric acid secretion.

The regulation patterns of gastric acid secretion in rats were investigated. Pentagastrin and histamine stimulate gastric acid secretion, but the inhibitors of DNA-dependent synthesis of RNA and of proteins prevent only the pentagastrin action. It has been found that pentagastrin induces histidine decarboxylase in gastric mucosa, ensuring local accumulation of histamine. The latter activates adenylate cyclase and results in 3',5'-AMP accumulation in gastric tissues. The administration of pentagastrin, histamine or 3',5'-AMP enhances the activity of gastric carbonic anhydrase, the enzyme which takes part in HCl formation. The data suggest that these three compounds act sequentially (pentagastrin leads to histamine leads to3',5'-AMP) and the effect of the last one could be mediated through 3',5'-AMP dependent protein kinase. The experiments in vitro demonstrated that gastric carbonic anhydrase can be separated into two isoenzymes and thephosphorylation of one of them by the 3',5'-AMP dependent protein kinase sharply increases its activity. The findings raise the possibility that histamine and 3',5'-AMP, mediating gastrin action, form together with enzymes (histidine decarboxylase, adenylate cyclase, protein kinase, carbonic anhydrase) a caascade of amplifiers. Autoradiographic studies have shown that [3H]-pentagastrin is not bound by oxyntic cells but adheres preferentially to histamine-producing alpha-like endocrine cells and to the chief cells, while 3H-histamine adheres preferentially to oxyntic and to chief cells. Electron microscopy indicates that only pentagastrin (but not histamine) initiates in alpha-like endocrine cells ultrastructural changes characteristic for induction. Pentagastrin, histamine and 3',5'-AMP administration produces in oxyntic cells ultrastructural changes typical for the secretion processes. These results lead to assumption that pentagastrin (gastrin) induces histidine decarboxylase in alpha-like endocrine cells of gastric glands. Histamine which is secreted enhances adenylate cyclase activity in the neighbouring oxyntic cells where 3',5'-AMP dependent protein kinase activates carbonic anhydrase by means of phosphorylation. These different cells form, probably, a multicellular functional unit for gastric acid secretion.

Adenosine Triphosphatases↗