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PubMed2004

[Clinico-pathogenetic variants of chronic gastritis].

AIM: To evaluate specific features of the course of chronic gastritis (CG), morphofunctional condition of gastric mucosa, vegetative regulation, adrenergic and cholinergic shifts, histamine metabolism and effects of exogenic and endogenic risk factors in CG patients; to study clinicopathogenetic variants of CG. MATERIAL AND METHODS: A total of 311 CG patients aged from 16 to 72 years were studied. They were divided into three groups by their gastric mucosa condition. The control group consisted of 30 healthy donors. The following parameters were studied: visual and histological condition of gastric mucosa, total acidity, the levels of free hydrochloric acid, pepsin, bioelectric gastric activity, general autonomic tonicity, cholinesterase activity. RESULTS: Three clinicopathogenetic variants of the disease have been identified. Variant 1 was characterized by a recurrent course, subjective manifestation of the disease only in exacerbation, surface (primarily antral) mucosal affection, normal or enhanced secretory and motor functions of the stomach, adequate reaction of acid production to caffeine and histamine stimulation, parasympathicotonia, absolute hyperhistaminemia, relative hypoacetylcholinemia, subnormal urinary excretion of adrenalin. Variant 2 manifested with rare recurrences, longer and more severe exacerbations, frequent spontaneous and provoked aggravations, moderate focal atrophy of the mucosa, secretory insufficiency with adequate reaction to histamine and minor to caffeine stimuli, hypomotor gastric dyskinesia, vegetative eutonia, normohistaminemia, absolute hypoacetylcholinemia, subnormal urinary excretion of noradrenaline. Variant 3 runs without definite remissions and exacerbations, with continuous abdominal pain and dyspepsia, frequent spontaneous aggravations, marked extended mucosal atrophy with secretory insufficiency up to achlorhydria, no stimulation of acid production in response to caffeine and histamine, gastric hypomotility, sympathicotonia, absolute hypohistaminemia, hypoacetylcholinemia, normal urinary excretion of catecholamines. CONCLUSION: The findings expand our knowledge about clinicopathogenetic variants of CG and necessitate new approaches to development of effective methods of CG prevention and treatment.

Acetylcholine↗
PubMedDate not supplied

Disposition of cyclosporine in several animal species and man. I. Structural elucidation of its metabolites.

Nine ether-extractable metabolites of cyclosporine were isolated from urine of dog and man and from rat bile and feces and purified by preparative HPLC and TLC. Structural assignments were mainly based on spectroscopic data (1H NMR, 13C NMR, MS) and the results of the amino acid analysis after hydrolysis with hydrochloric acid. All the identified metabolites retained the intact cyclic oligopeptide structure of the parent drug. Structural modifications originated from enzymatic oxidation at specific sites of the peptide subunits. Transformation processes principally involved hydroxylation at the terminal carbon atom (eta-position) of the C9-amino acid 1 and the gamma-position of the N-methylleucines 4, 6, and 9, as well as N-demethylation of the N-methylleucine 4. Regioisomeric monohydroxylated cyclosporines (metabolites 1, and 17) and N-demethylcyclosporine (metabolite 21) were the primary metabolites resulting from hydroxylation of the C9-amino-acid 1 and the N-methylleucine 9, and from N-demethylation of the N-methylleucine 4. Dihydroxylated derivatives of cyclosporine (metabolites 8, 10, and 16) were generated by further oxidation of metabolite 1 on one of the other N-methylleucines (4 or 6) or on the C9-amino acid 1, or of metabolite 17 on the N-methylleucine 9. More extensive modifications were observed for metabolite 9, a dihydroxy-N-demethylcyclosporine, which could have been formed from the dihydroxy derivative 16 by N-demethylation or from the N-demethylcyclosporine 21 by dihydroxylation. Metabolite 18 differed from 17 (monohydroxycyclosporine) by the presence of a cyclic ether moiety, formally derived by intramolecular addition of the beta-hydroxyl group to the double bond of the C9-amino acid 1.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1978

Interlaboratory comparison of results of erythrocyte protoporphyrin analysis.

Each of 65 laboratories analyzed 10 whole-blood samples for erythrocyte protoporphyrin by one or more of several analytical procedures. These procedures were of two types: (a) extraction of protoporphyrin from the erythrocytes into ethyl acetate/acetic acid, re-extraction into hydrochloric acid, and fluorometric measurement; or (b) direct reading in a portable fluorometer (hematofluorometer), with no pretreatment of the blood sample. Interlaboratory correlation was generally poor, especially between laboratories using extraction procedures. Hematofluorometric results intercorrelated better, but they had a low bias as compared to the extraction approach. Nationwide standardization of the test is required to assure satisfactory interlaboratory performance and to identify laboratories whose results are sufficiently accurate to be used for interpretations according to guidelines set forth by the Center for Disease Control for erythrocyte protoporphyrin testing.

Analysis of Variance↗
PubMed1998

Experimental study of acid burden and acute oesophagitis.

BACKGROUND: The relationship of the pH of oesophageal refluxate and its pepsin content to injury of oesophageal mucosa remains unclear. A study was made of the earliest morphological alterations in the oesophageal mucosa secondary to varying concentrations of hydrochloric acid with or without pepsin. METHODS: Adult cats had varying concentrations of acid with and without 1 per cent porcine pepsin infused into the oesophagus through a paediatric feeding tube placed 5 cm above the oesophagogastric junction at a rate of 1 ml/min for 30 min. At autopsy 24 h later, the oesophagus was removed intact and scored by an expanded modification of a previously published histopathological scoring system. This included estimates of the intensity and distribution of four morphological features: basal cell hyperplasia (BCH), intraepithelial leucocytes (IELs), subepithelial leucocytes and ulcers. Each of these four categories was scored from 0 to 4, with a maximum injury score of 16. RESULTS: Mean(s.e.m.) scores were as follows: pH 1, 15.0(1.0); pH 1 with pepsin, 13.3(1.4); pH 2, 15.3(0.7); pH 2 with pepsin, 11.7(1.1); pH 3, 1.8(1.6); pH 3 with pepsin, 3.7(1.9); pH 4 with or without pepsin, 0.6(0.2). Differences between pH 3 and 4 versus pH 1 and 2 were significant (P < 0.05). CONCLUSION: Injury to the oesophagus is more dependent on the pH of refluxate than on the presence of pepsin. Peptic injury appears to occur at a critical threshold of acid burden (pH < 3) as opposed to a graded level of injury based on a pH scale.

Acute Disease↗
PubMed1990

Mechanism of acid-induced release of secretin in rats. Presence of a secretin-releasing peptide.

In fasting rats, intraduodenal infusion of dilute hydrochloric acid results in significant increases in both pancreatic exocrine secretion and plasma concentration of secretin. To test the hypothesis that acid-induced release of secretin is mediated by a secretin-releasing factor (S-RF), anesthetized rats were prepared with pyloric ligation, duodenal and jejunal cannulas, and pancreatic duct cannulas. Donor rats were infused intraduodenally with 0.01 N HCl, 0.15 M NaCl, or a combination of 0.01 N HCl and 0.05 N NaHCO3 at 0.3 ml/min for 1.5 h, and the perfusates were collected via jejunal cannulas. The perfusates with pH adjusted to 6.0 were concentrated threefold and infused into the duodena of recipient rats. The concentrate of acid perfusate (CAP) significantly increased both pancreatic volume flow and bicarbonate output and plasma concentration of secretin, whereas concentrates of the saline perfusate (CSP) or the perfusate of a combination of 0.01 N HCl and 0.05 N NaHCO3 (CABP) did not influence pancreatic secretion or plasma concentration of secretin. The increased pancreatic secretion by CAP was attributed to increased circulating secretin because when secretin was immunoneutralized by a rabbit antisecretin serum, CAP-stimulated pancreatic secretion was abolished. The bioactivity of CAP was trypsin-sensitive and heat stable. The active substance in CAP had a molecular weight of less than 5,000 and greater than 1,000, as determined by ultrafiltration and bioassay. In conclusion, dilute HCl releases an S-RF into the upper small intestinal lumen to stimulate release of secretin. This substance, with molecular weight of less than 5,000, is heat stable and trypsin sensitive. Thus, the acid-stimulated release of secretin is mediated by a secretin-releasing peptide in the upper small intestinal lumen.

Animals↗
PubMed2002

An improved method for production of silica from rice hull ash.

Rice hull ash (RHA) contains over 60% silica and can be an economically viable raw material for the production of silica based products. A previously published method for producing silica xerogel involved dissolving RHA silica with alkali solution to form sodium silicate solution and subsequently forming silica aquagel by adding hydrochloric acid to lower the pH from 11.8 to 7.0, followed by washing and drying aquagel to form xerogel. The silica xerogel had over 4% sodium as a contaminant. An improved method to produce silica xerogel with lower sodium is described in this study. The improved method involved production of silica aquagel by adding silicate solution to pH 1.5 hydrochloric, citric, or oxalic acid solutions until the pH 4.0 was reached. The aquagel was washed and dried to form silica xerogel. For comparison silica xerogels were also produced at pH 7.0 by the published method. X-ray photoelectron spectroscopy was used to determine the elemental content of silica xerogels. The silica, sodium, carbon and oxygen content of silica xerogels varied depending on the pH and the type of acid used for the production of these xerogels. Silica xerogels produced by the improved method using citric and oxalic acid had sodium content of 0.52% and 0.22%, respectively.

Acids↗
PubMed1995

Studies on antiulcer agents. III. Plausible mechanism of antisecretory action of ethyl 2[(1H-benzimadazol-2-yl)sulfinylmethyl]-4-dimethylamino- 5-pyrimidinecarboxylate, an H+/K(+)-ATPase inhibitor, based on its reaction with thiols.

To explore the mechanism of the gastric antisecretion activity of ethyl 2-[(1H-benzimidazol-2-yl)sulfinylmethyl]- 4-dimethylamino-5-pyrimidinecarboxylate (5), a potential H+/K(+)-ATPase inhibitor, in the acid compartment of parietal cells, its reaction with some alkylthiols in the presence of hydrochloric acid was investigated. Upon treatment with 2-mercaptoethanol under acidic conditions, 5 gave a characteristic 1:2 adduct, ethyl 4-[2-(2-hydroxyethyldithio)- 1-(2-hydroxyethylthio)ethylidenamino]pyrimido[1,2-a]benzimid azole-3- carboxylate (6), instead of providing a disulfide of type 3, 2-(2-alkyldithiomethylpyridino)benzimidazolide, the product predicted to be formed according to the reaction mechanism of common H+/K(+)-ATPase inhibitors, such as omeprazole or lansoprazole, with mercaptans. With a large excess of 2-mercaptoethanol, 5 provided 2-(2-hydroxyethylthio)-1H-benzimidazole (8) and ethyl 4-dimethylamino-2-(2-hydroxyethyldithio)-5-pyrimidinecarboxylat e (9) as well as 6. The transformation mechanisms and their implications are discussed.

Anti-Ulcer Agents↗
PubMed2001

The role of substance P release in the lung with esophageal acid.

To investigate whether tachykinins are released in the airways by stimulating the esophagus, airway plasma extravasation induced by intraesophageal hydrochloric acid (HCl) in the presence or absence of the neutral endopeptidase (NEP) inhibitor phosphoramidon and the neurokinin-1-receptor antagonist FK888 was studied in anesthetized guinea pigs. Airway plasma extravasation also was studied in the presence of the NEP inhibitor in guinea pigs pretreated with capsaicin or bilateral vagotomy. Propranolol and atropine were used in all animals to block adrenergic and cholinergic nerve effects. Airway plasma leakage was evaluated by measuring extravasated Evans blue dye. One normal HCl infusion into the esophagus significantly increased plasma extravasation in the trachea. Phosphoramidon significantly potentiated plasma extravasation induced by HCl infusion into the esophagus in the trachea and main bronchi, and FK888 significantly inhibited extravasation in a dose-related manner. In capsaicin-treated animals, airway plasma extravasation was completely inhibited even in the presence of phosphoramidon. Tracheal plasma extravasation potentiated by phosphoramidon was significantly inhibited in the bilaterally vagotomized animals. These results suggest that locally acting substances are released by intraesophageal HCl stimulation that cause airway plasma extravasation. These substances are generated through activation of neural pathways, including some that traffic through the vagus nerves that link the esophagus or airways.

Animals↗
PubMed1994

Hyperventilation in the treatment of metabolic acidosis does not adversely affect pulmonary gas exchange.

BACKGROUND: Hyperventilation has been recommended to increase blood pH during metabolic acidosis. However, hypocapnia may adversely affect arterial blood oxygenation, especially in the presence of lung disease. We therefore studied the effects of metabolic acidosis, with and without normalization of pH by hyperventilation, on pulmonary gas exchange in dogs with permeability pulmonary edema. METHODS: Six pentobarbital-anesthetized dogs were administered 0.06 ml/kg of oleic acid at least 150 min before study. Ventilation was set with an inspired O2 fraction of 0.90 and a tidal volume of 18 ml/kg, and the respiratory rate was adjusted to alter the arterial CO2 tension (PaCO2) per the experimental protocol. The protocol in random order was (1) normal pH (7.36 +/- 0.01)/normal PaCO2 (39 +/- 1 mmHg); (2) low pH 7.20 +/- 0.01)/normal PaCO2 (40 +/- 1 mmHg); (3) low pH (7.18 +/- 0.01)/hyperventilation with inspired CO2 (PaCO2 = 40 +/- 1 mmHg); and (4) normal pH (7.35 +/- 0.01)/hyperventilation with low PaCO2 (24 +/- 1 mmHg). In phases 2-4, the pH was slowly reduced by intravenous infusion of 2 N hydrochloric acid. The pH was normalized in phase 1 where necessary by infusion of sodium bicarbonate. The pH in phase 4 was normalized by reducing the PaCO2 by increasing the respiratory rate. Gas exchange was assessed by the multiple inert-gas elimination technique. RESULTS: The hemodynamic measurements remained constant throughout the protocol. Arterial O2 tension increased from 244 +/- 55 to 293 +/- 49 mmHg in the presence of metabolic acidosis (P < 0.05). Hyperventilation to normalize the pH during metabolic acidosis (phase 4), increased arterial O2 tension (313 +/- 44 mmHg, P < 0.05), and reduced shunt (from 20 +/- 5% to 12 +/- 3%, P < 0.05) compared with normal acid-base conditions (phase 1). No change in shunt was observed with hyperventilation compared with metabolic acidosis alone (phase 2). The decrease in pulmonary shunt was not attributable to the direct effects of hyperventilation, because shunt was increased (20 +/- 5%) when PaCO2 was normalized during hyperventilation by inspiration of CO2 (phase 3). CONCLUSIONS: Hyperventilation to normalize blood pH during hydrochloric acid-induced metabolic acidosis did not adversely affect pulmonary gas exchange in dogs with permeability pulmonary edema.

Acidosis↗
PubMed1969

Effect of acid infusion into various levels of the intestine on gastric and pancreatic secretion in the cat.

Intraduodenal infusion of increasing amounts of hydrochloric acid solution results in a stepwise increase in the volume of pancreatic secretion and output of bicarbonate, reaching about 90% of amounts attained with exogenous secretin infused intravenously in increasing doses. Acid infusion into the different regions of the intestine stimulates pancreatic secretion only from the duodenum and upper jejunum, suggesting that the area of endogenous release of secretin by acid is confined to the upper part of the small bowel in the cat. Gastric acid secretion induced by pentagastrin, but not by histamine, is inhibited by acid perfusion of the duodenum. The acidification of other parts of the small intestine does not result in any change in gastric acid secretion induced either by pentagastrin or by histamine.

Animals↗
PubMed1996

The effect of atrial natriuretic peptide on pulmonary acid injury in a pig model.

The effect of exogenous atrial natriuretic peptide (ANP) on pulmonary injury induced by aspiration of hydrochloric acid (0.1 N HCl, 2.0 ml/kg) was examined in anesthetized pigs ventilated with 100% oxygen. Group-specific diuretic treatment was used 60 min after aspiration and followed for a further 120 min. No diuretics were used for Group 1, 0.1 microg/kg/min of ANP was infused intravenously for 60 min in Group 2, and 0.05 mg/kg of furosemide was injected (intravenous bolus) in Group 3. Total urine volume after diuretic treatment did not differ significantly between Groups 2 and 3. However, the increase in PaO2 (to 386.3 +/- 67.5 mm Hg) after infusion of ANP was significantly higher than the increase in PaO2 (to 275.9 +/- 63.3 mm Hg) after furosemide treatment, and in the no treatment control (to 171.1 +/- 31.5 mm Hg). Pulmonary hypertension induced by acid aspiration was significantly reduced (p < 0.01 versus Groups 1 and 3) during ANP infusion. ANP has a beneficial effect on acute lung injury, possibly through its diuretic and/or pulmonary vasodilating action.

Animals↗
PubMed1985

Mechanisms underlying the intestinal fluid secretion evoked by nociceptive serosal stimulation of the rat.

Intestinal net fluid transport was measured in vivo continuously with a gravimetric method. Chemical stimulation of the jejunal serosa with hydrochloric acid (0.1 M), ethanol (20%), cat bile or 7-deoxycholic acid (10 mM) evoked an intestinal fluid secretion. Hexamethonium (10 mg/kg b.wt.i.v.) or serosal application of lidocaine (1% solution) partially blocked this secretory response. Bradykinin and prostaglandin E1, two important inflammatory mediators, elicited fluid secretion when applied to the serosal surface at a concentration of 10(-4) M. This secretion was also partly inhibited by hexamethonium. Furthermore indomethacin (10 mg/kg b.wt. i.v.) or pyrilamine (10 mg/kg b.wt. i.v.), a H1-receptor blocker, partly inhibited the secretory response caused by chemical stimulation of the serosa while cimetidine (1 mg/kg b.wt. i.v.), a H2-receptor blocker, had no effect. Freeze sectioned samples from chemically stimulated intestines were examined by fluorescence microscopy. A leakage of i.v. administrated Evans blue labelled albumin into the interstitial space of the serosa and the outer layer of the muscularis was found. It is concluded: The intestinal fluid secretion studied is mainly elicited by nociceptive stimulation of nerves in the serosa or the outer muscularis. The reflex may be activated by the local release of histamine, kinins and prostaglandins. The reflex studied is part of an inflammatory response.

Animals↗
PubMed1971

Sporulation in Bacillus subtilis 168. Comparison of alkaline phosphatase from sporulating and vegetative cells.

1. The purification of the ;vegetative' alkaline phosphatase of Bacillus subtilis 168 was simplified by ionic elution of the enzyme from intact cells. 2. The enzyme has a molecular weight of about 70000 and treatment of the enzyme with 10mm-hydrochloric acid or 6.0m-guanidine hydrochloride, beta-mercaptoethanol (0.1m) gives rise to enzymically inactive subunits. 3. The amino acid composition of the enzyme was determined. The N-terminal residue determined by the DNS chloride method is glycine. 4. The properties of this enzyme were compared with the ;sporulation' alkaline phosphatase of the same strain. 5. Although the ;sporulation' enzyme differs from the ;vegetative' enzyme in its physiology of appearance and apparent mRNA stability, an examination of properties of the enzymes revealed no differences. 6. The enzyme from both cell forms is bound to the particulate fraction of cell extracts, but can be solubilized by high concentrations of magnesium chloride; removal of the magnesium chloride, by dialysis, results in precipitation of both enzymes. Both enzymes can be removed from intact cells by ionic elution. 7. The ;vegetative' and ;sporulation' enzymes have identical pH optima, K(m) and K(i) values and electrophoretic mobilities in cellulose acetate. 8. Their half-life is 28min at 65 degrees C and their Q(10) is 1.25. 9. The molecular size determined by gel filtration on Sephadex G-100 is about 69000. 10. ;Vegetative' and ;sporulation' forms gave precipitin lines that were continuous and non-spurred when tested against antiserum prepared against the ;vegetative' enzyme. 11. The ;sporulation' alkaline phosphatase appears to be associated with stage II of sporulation and appears to be induced by something specifically concerned in sporulation and not by phosphate starvation.

Alkaline Phosphatase↗
PubMed1994

In vitro buffering capacities of proprietary non-particulate antacids available in New Zealand.

Four commercially available non-particulate antacid preparations were titrated against 1M hydrochloric acid to assess buffering capacity as compared to 30 ml 0.3M sodium citrate solution. All antacids were used in the manufacturers "unit dose". All antacids tested demonstrated some in vitro buffering capacity, and "Eno" (Reckitt and Colman) had a buffering capacity similar to that of sodium citrate. The retail cost per unit dose was established for each proprietary antacid and for sodium citrate. It was concluded that while proprietary antacids are cheaper per dose than sodium citrate, preparations differ in their acid-neutralising capacity.

Antacids↗
PubMed1982

Role of a secretagogue immunoglobulin in gastric acid secretion.

Results of this study showed that in a considerable number of patients with duodenal ulcer a globulin of the IgG class was responsible for the enhancement of HCl secretion. This secretagogue globulin appeared to combine directly with the H2 receptors of the parietal cells thereby increasing hydrochloric acid output without the formation of antigen-antibody complex.

Anemia, Pernicious↗
PubMed1983

Generation of chemotactic activity in normal guinea pig serum by treatment with acid.

Chemotactic activity was generated in normal guinea pig serum following titration of the pH to 4 by the addition of hydrochloric acid. The process was time and temperature dependent. The chemotactic material was stable when kept at pH 4, but decayed within one or two days when the pH was raised to neutrality. Fractionation of the acid-treated serum by Sephacryl S-200 gel filtration revealed two peaks of activity, one eluting with molecules larger than bovine serum albumin, the other in the 13,000 MW range. After heating the serum at 56 degrees C for 60 min no chemotactic activity could be generated by acid, while EDTA, EGTA, hydrazine and the enzyme inhibitors benzamidine, EACA, PMSF, and pepstatin, added to the serum prior to the addition of acid, had no effect. The results suggest that chemotactic factors, remarkably similar to the products of complement activation, could be generated in guinea pig serum by a mechanism differing from the classical or the alternative complement activation pathways.

Animals↗
PubMed1979

Impaired acid neutralization in the duodenum in pancreatic insufficiency.

The influence of severe exocrine pancreatic disease on the acid-neutralizing capacity of the duodenum was studied in five patients with pancreatic insufficiency (PI) and six control subjects using duodenal perfusion-marker technique. Hydrochloric acid (0.1 N containing 1% PEG) was infused at constant rates (1.2, 4.5 and 7.0 ml/min) into the duodenum just distal to the duodenal bulb. Samples were aspirated from the tip of the duodenal perfusion tube located at the ligament of Treitz. All samples were analyzed for volume, pH, titrable acidity, PEG and [14C]PEG (gastric marker) determination. Patients with PI demonstrated significantly diminished ability to neutralize various acid loads as compared to controls who virtually completely neutralized acid loads in the range of maximal gastric acid secretion. Exogenous secretin did not significantly improve percent acid neutralized in PI. These data clearly indicate that patients with PI have significantly impaired ability to neutralize even small loads of acid in the duodenum.

Bicarbonates↗