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PubMed1985

Ammonia transport by the turtle bladder: relationship to H+ secretion.

The turtle bladder is apparently capable of transporting ammonia in the form of NH3 as well as NH+4. In the present study we examined the relationship of ammonia transport into the mucosal solution to H+ secretion and to chemical reactions in the unstirred layers. The relationship between ammonia transport and H+ secretion was examined before and after inhibition of H+ secretion by acetazolamide, SITS, and the putative inhibitor of the H+ pump dicyclohexylcarbodiimide. All these inhibitors caused a significant decrease in H+ secretion and led to a parallel decrease in the rate of ammonia transport with serosal pH at 6.4. Stimulation of H+ secretion by 1% CO2 increased both H+ secretion and ammonia transport at serosal pH 6.4. At serosal pH 6.4 the changes in H+ secretion were highly correlated with changes in ammonia transport. Ammonia transport at serosal pH 6.4 was electrogenic and inhibited by a low mucosal pH. In contrast, the diffusion of NH3 down an imposed concentration gradient was not correlated with changes in H+ secretion. Chemical reactions in the unstirred layers seem to influence ammonia transport in that increasing serosal nonvolatile buffer concentrations decreased the diffusion of NH3 down the concentration gradient from the serosal into the mucosal solution, probably by decreasing serosal NH3 concentration. Conversely, addition of uncouplers in the mucosal solution in an attempt to decrease the H+ concentration in the mucosal solution unstirred layer decreased the ammonia transport at serosal pH 6.4.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed1985

Ammonia and bicarbonate transport by rat cortical collecting ducts perfused in vitro.

We measured bicarbonate and ammonia transport by isolated perfused cortical collecting ducts from deoxycorticosterone-treated rats. With no ammonia in the perfusate and bath solutions, the collecting ducts secreted bicarbonate. The bicarbonate secretion was prevented when the rats were given 40 mM NH4Cl to drink. When 4 mM total ammonia was added to the perfusate and bath, the collecting ducts secreted ammonia and the direction of bicarbonate transport reversed toward absorption. Under those conditions the collected total ammonia concentration exceeded the value predicted by the diffusion-trapping model, assuming pH equilibrium. However, when carbonic anhydrase was added to the perfusate (to assure pH equilibrium), the collected total ammonia concentration decreased to the level predicted by the diffusion-trapping model. We conclude that rat cortical collecting ducts can secrete bicarbonate at substantial rates; the rate of bicarbonate secretion is modified by changes in the acid-base intake of the rats; ammonia secretion occurs by simple nonionic diffusion in this segment; the ammonia secretion is enhanced by the presence of acidic pH disequilibrium in the lumen; and ammonia in the perfusion and bath solutions inhibits bicarbonate secretion by rat cortical collecting ducts, a response that may be important for the regulation of renal bicarbonate excretion.

Ammonia↗
PubMed1992

Effects of barium and 5-(N-ethyl-N-isopropyl)-amiloride on proximal tubule ammonia transport.

Ionic NH+4 transport is an important mode of ammonia transport in the proximal convoluted tubule (PCT). NH+4 transport via the Na-H exchanger has been previously demonstrated. Potassium channels are present in the proximal tubule, but their role in ammonia transport has not been evaluated. We studied rat PCTs perfused in situ at 30 nl/min with solutions containing 5 mM HCO3; ammonia was measured with a fluorometric method. When perfused with the potent amiloride analogue 5-(N-ethyl-N-isopropyl)-amiloride (EIPA, 500 microM) or with BaCl2 (10 mM), ammonia entry (14.3 +/- 1.7 and 11.8 +/- 1.5 pmol.min-1.mm-1, respectively) was unaffected compared with control (12.8 +/- 1.0 pmol.min-1.mm-1). However, the combination of EIPA and barium inhibited entry (7.4 +/- 1.0 pmol.min-1.mm-1, P less than 0.02 vs. other groups). Also, when perfused with 10 mM ammonia, neither EIPA nor BaCl alone blocked ammonia loss (70.5 +/- 9.1 and 60.5 +/- 5.9 pmol.min-1.mm-1, respectively) compared with control (53.4 +/- 6.0 pmol.min-1.mm-1). However, the combination inhibited ammonia loss (29.2 +/- 6.3 pmol.min-1.mm-1, P less than 0.025 vs. other groups). Thus blocking both the Na-H exchanger and potassium channels decreases PCT ammonia transport. As the combination was required, this implies that multiple pathways exist for NH+4 transport in the PCT. This is the first demonstration that a mode of NH+4 transport other than via the Na-H exchanger is important in this segment, and the data are most consistent with transport of ammonia via potassium channels.

Amiloride↗
PubMed1983

Tissue ammonia and amino acids in rats at various oxygen pressures.

The amino acid and ammonia profiles in various tissues of the rat exposed to different pressures of pure oxygen have been studied. Well-defined changes in behavioral activity accompanied a profile of increasing pressure, culminating in convulsive activity in each group of exposed animals. After an initial depression of ammonia, in all tissues studied at 0.68 atm oxygen ammonia increased significantly at higher oxygen pressures. A rise in tissue ammonia took place in the absence of undue muscular activity on the part of the exposed animals. A significant increase in ammonia occurred first in brain and liver at 3.40 atm. Ammonia concentration was high in all tissues after convulsions occurred at 4.08 atm. Between 0.68 and 2.72 atm oxygen, tissue ammonia concentration was generally low and brain glutamate and gamma-aminobutyric acid were high. At pressures higher than 2.72 atm oxygen, tissue glutamate declined and glutamine increased. Alanine became significantly elevated in serum and muscle at high oxygen pressure, and aspartate was depressed in heart, liver, and muscle. These pressure-course experiments on ammonia accumulation in tissue confirm previous serial time course observations that ammonia accumulates in the brain and several tissues of the rat even in the absence of undue muscular activity during high-pressure oxygen exposure and is a significant factor in inducing convulsions.

Amino Acids↗
PubMed2004

Maternal and fetal blood ammonia concentrations in normal term human pregnancies.

BACKGROUND: The current evidence on the primary source of ammonia production in the human fetoplacental unit is potentially misleading. OBJECTIVE: The aim of the present investigation was to determine the concentration of ammonia in human maternal and fetal blood at birth and to compare them with published data in late gestation sheep. METHODS: In 12 normal human pregnancies, umbilical arterial and venous and maternal venous blood was sampled, and whole blood ammonia concentrations were measured. Data from 12 pregnant sheep and fetuses from our previous studies were utilized for comparison. RESULTS: The human fetus at delivery has higher concentrations of ammonia (60-80 microM) than the late gestation fetal lamb (25-35 microM). In the human, the arterial umbilical ammonia concentration exceeds the venous umbilical concentration, indicating a net ammonia production by fetal tissues. In sheep, the venous umbilical ammonia concentration exceeds the arterial umbilical concentration, indicating the net placental ammonia production. CONCLUSIONS: In contrast to fetal lambs, human fetuses exhibit a net production of ammonia, which may reflect differences in biologic state or a species difference.

Adult↗
PubMed1981

Effect of intralumenal cation-exchange resin on excretion of ammonia in rat ileum.

Ammonia excretion was studied in rat ileal segments during perfusion of the animal through the saphenous vein. In the first 10 min during and after intravenous infusion of L-glutamine (116 mg/kg to double arterial glutamine concentration) average net change in lumenal ammonia was 13 +/- 8 (S.E.) nmole NH3/min/g ileum; average net change in ileal venous ammonia was 28 +/- 9 nmole NH3/min/g ileum; and average net change in total ammonia (lumen + ileal vein) was 41 +/- 13 compared to -5 +/- 10 nmole/min/g ileum for animals infused with saline P less than 0.025. These data suggest that ileal metabolism of arterial glutamine liberates ammonia to both ileal venous blood and intestinal lumen. When a cation-exchange resin which binds ammonia was infused intralumenally, average net change in lumenal ammonia in the first 10 min during and after intravenous infusion of 116 mg/kg L-glutamine was 415 +/- 156 nmole NH3/min/g ileum (p less than 0.01 compared to value during perfusion of Earle's solution alone). During the first 10 min during and after glutamine infusion net change in ileal venous plasma ammonia was -8 +/- 14 when resin was being perfused through the lumen compared to +28 +/- 9 nmole/min/g ileum during perfusion of Earle's solution alone without resin P less than 0.05. Thus resin in the small intestine can trap very large amounts of ammonia.

Ammonia↗
PubMed2001

Effects of ammonia on acid-base transport by the B-type intercalated cell.

Ammonia, in addition to its role as a constituent of urinary net acid excretion, stimulates cortical collecting duct (CCD) net bicarbonate reabsorption. The current study sought to begin determining the cellular transport processes through which ammonia regulates bicarbonate reabsorption by testing whether ammonia stimulates B-type intercalated cell bicarbonate secretion, bicarbonate reabsorption, or both. The effects of ammonia on single CCD intercalated cells was studied by use of measurements of intracellular pH taken from in vitro microperfused CCD segments after luminal loading of the pH-sensitive fluorescent dye BCECF. These results showed, first, that ammonia inhibited B-cell unidirectional bicarbonate secretion and that this occurred despite no effect of ammonia on apical Cl(-)/HCO(3)(-) exchange activity. Second, ammonia increased the contribution of a SCH28080-sensitive apical H(+)-K(+)-ATPase to basal intracellular pH regulation and it stimulated basolateral Cl(-)/HCO(3)(-) exchange activity. Thus, ammonia activated both apical proton secretion and basolateral base exit, consistent with stimulation of unidirectional bicarbonate reabsorption. It was concluded that ammonia regulates CCD net bicarbonate reabsorption, at least in part, through the coordinated regulation of the separate processes of B-cell bicarbonate reabsorption and bicarbonate secretion. These effects do not reflect a general activation of ion transport but, instead, reflect coordinated and specific regulation of ion transport.

Absorption↗
PubMed2003

Water quality guidance for protection of freshwater mussels (Unionidae) from ammonia exposure.

Ammonia toxicity data for freshwater mussels (Unionidae), a significantly imperiled taxa, were used to derive estimates of concentrations that would not likely be harmful in acute and chronic exposures and to assess the protectiveness of current U.S. Environmental Protection Agency (U.S. EPA) water quality criteria to this family of organisms. Thirty acute (24-96-h) median lethal concentrations (LC50s), covering 10 species in eight unionid genera, were used to calculate genus mean acute values (GMAVs) ranging from 2.56 to 8.97 mg/L total ammonia as N at pH 8. Freshwater mussels are at the sensitive end of the range when added to the GMAVs from the database used to derive the U.S. EPA criteria maximum concentration (CMC). We derived two estimates of acute exposure water quality guidance for the protection of freshwater mussels (CMC(FM)) by a recalculation of the CMC after adding freshwater mussel GMAVs to the U.S. EPA data set. The CMC(FM)s of 1.75 and 2.50 mg/L total ammonia as N at pH 8 average 60% less than the U.S. EPA CMC of 5.62 mg/L total ammonia as N at pH 8 for application when salmonids are present. These values average about 75% less than the CMC for application when salmonids are absent. No chronic ammonia exposure data existed for unionids. Thus, we applied a range of estimated acute:chronic ratios to the acute toxicity data set, expanded with the freshwater mussel GMAVs. to estimate continuous ammonia concentrations that may be protective of freshwater mussels. These estimates ranged from 0.3 to 1.0 mg/L total ammonia as N at pH 8, about 20 to 75% less than the U.S. EPA criteria continuous concentration (CCC) of 1.24 mg/L total ammonia as N at pH 8 and 25 degrees C. The current numeric criteria for ammonia may not be protective of mussels, more than half of whose nearly 300 species are in decline in North America. While the CMC(FM) and CCC(FM) are not equivalent to revised U.S. EPA criteria, they are offered as interim guidance for the protection of freshwater mussels.

Ammonia↗
PubMed2006

Reducing crude protein in beef cattle diet reduces ammonia emissions from artificial feedyard surfaces.

Concentrated animal feeding operations are major sources of ammonia to the atmosphere. Control methods to reduce emissions include acidifying amendments, urease inhibitors, and absorbents. For beef cattle, decreasing crude protein (CP) in diets may be the most practical and cost-effective method to reduce ammonia emissions. Our objective was to quantify the effect of reducing CP in beef cattle diet on ammonia emissions. Two groups of steers were fed diets with either 11.5 or 13.0% CP and all urine and feces were collected. Manures from the two diet treatments were applied in a replicated laboratory chamber experiment, and ammonia emission was quantified using acid gas washing. In four seasonal field trials, manures from the two diet treatments were applied to two 10-m-diameter, circular, artificial feedyard surfaces, and ammonia emission was quantified using the integrated horizontal flux method. Manure from steers fed 11.5% CP diet had less urine, less urinary N, and a lesser fraction of total N in urine, compared with the 13.0% CP diet. Decreasing crude protein in beef cattle diets from 13 to 11.5% significantly decreased ammonia emission by 44% (p < 0.01) in the closed chamber laboratory experiment, and decreased mean daily ammonia flux by 30% (p = 0.10), 52% (p = 0.08), and 29% (p < 0.01) in summer, autumn, and spring field trials, respectively. No difference was observed in winter. On an annual basis, decreasing crude protein reduced daily ammonia flux by 28%. Reducing crude protein in beef cattle diets may provide the most practical and cost-effective way to reduce ammonia emissions from feedyards.

Air Pollutants↗
PubMedDate not supplied

Ammonia inhibition in the anaerobic treatment of fishery effluents.

Inhibition of the organic matter consumption rate of a saline and rich proteic effluent by free ammonia was assessed in anaerobic filters at 37 degrees C. Inhibition of substrate (total organic carbon, TOC) consumption rate by ammonia was fitted by the Luong and noncompetitive models. Calculated kinetic parameters using the Luong model were maximum specific growth rate, micromax = 0.28 day(-1); average saturation constant, Ks = 568 mg TOC/L; Luong inhibition parameter, KNH3 = 1707mg ammonia-nitrogen (NH3-N)/L; and Luong exponent, gamma = 0.283 and the noncompetitive calculated parameters were umax= 0.26 day(-1), Ks = 703 mg TOC/L, and inhibition parameter, INH3 = 325 mg NH3-N/L. The Luong and noncompetitive models predicted 50% inhibition of the substrate consumption rate at ammonia concentrations of 147 and 325 mg NH3-N/L, respectively, suggesting biomass adaptation to the ammonia concentration (80 mg NH3-N/L as average) at which the anaerobic filters were previously operating. Ammonia formation by anaerobic digestion of fishing effluent would produce a maximum of 65.1 and 58.6% inhibition of the efficiency, predicted by the Luong and noncompetitive models, respectively. Ammonia influence on the digestion steps was determined by comparing fishing effluent with volatile fatty acids as substrates. The noncompetitive model predicted a 50% inhibition of methane production rate at ammonia concentrations of 196.6 and 188.6 mg NH3-N/L for fishing effluent and volatile fatty acids, respectively, suggesting that the methanogenic step is the one most affected by ammonia.

Ammonia↗
PubMed2001

Dietary manipulation to reduce aerial ammonia concentrations in nursery pig facilities.

Two 4-wk trials (preliminary study) and three 5-wk trials (major study) were conducted to determine the effects of adding Yucca schidigera extract or anhydrous calcium chloride to nursery diets on the growth performance of nursery pigs and aerial ammonia concentration. The pigs were weaned between 13 and 15 d of age and had an initial BW of 3 to 6 kg. In each trial, pigs were allotted to three identical pig nursery rooms that were environmentally regulated. There were three diets (one diet per room): 1) control, containing 23% CP; 2) control plus 125 ppm of Yucca schidigera extract; and 3) control plus 1.95% anhydrous calcium chloride. Growth performance was recorded weekly. Aerial ammonia concentration was measured daily using aspiration detector tubes and during the last week of each trial using diffusion tubes. Manure samples were collected twice a week during the experimental period to determine ammonia and N concentrations and pH. Plasma urea concentration was determined in blood samples collected from the pigs at the end of each trial. Data were analyzed using split-plot and Latin square designs for the preliminary and major studies, respectively. Feed intake was similar among pigs fed all three diets. There were no differences in ADG and ADG/ADFI (G/F) between pigs fed the control diet and pigs fed the yucca extract diet (P > or = 0.41). In all trials, pigs fed the calcium chloride diet had lower ADG and G/F than pigs fed the other two diets (P < 0.05). In the preliminary study, aerial ammonia tended to be greater in the rooms in which pigs were fed the control diet than in the rooms with pigs fed the yucca extract diet (P = 0.08) and the calcium chloride diet (P = 0.11). In the major study, aerial ammonia increased weekly (diet x week; P < 0.001) in all rooms. In the 4th wk, ammonia concentrations were greater (P < 0.001) in the rooms in which pigs were fed the control diet than in the rooms in which the other two diets were fed. Dietary treatment had no effect on plasma urea concentration (P > or = 0.10), manure ammonia and N concentrations (P > or = 0.50), and manure pH (P > or = 0.78). Although aerial ammonia concentrations were relatively low, the addition of Yucca schidigera extract or calcium chloride to the diet of nursery pigs reduced ammonia concentrations in the nursery rooms.

Air Pollutants↗
PubMed2001

Dietary adipic acid reduces ammonia emission from swine excreta.

Adipic acid is only partially catabolized when it is fed to animals, and a portion of it is excreted in urine. The excreted portion may lower urinary pH and, as a result, ammonia emission. The present study tested this hypothesis. In Exp. 1, nursery pigs (n = 14) were fed (for a period of 7 d) either a standard nursery diet or the same diet supplemented with 1% adipic acid to assess effects on urinary pH (collected on d 5 or 6) and in vitro ammonia emission from the collected urine samples that were mixed with control feces. In Exp. 2, grower pigs housed 10 each in one of two chambers were fed a control diet or the same diet supplemented with 1% adipic acid. Ventilated air was quantified and analyzed for ammonia using Fourier transform infrared spectroscopy to determine the effects of feeding 1% adipic acid on ammonia emission. The results from Exp. 1 showed that adipic acid strongly reduced urinary pH (from 7.7 to 5.5, P < 0.05). In vitro ammonia emission from these urine samples was significantly reduced at all the time points evaluated (1, 3, 18, and 46 h with reductions of 94, 93, 70, and 39%, respectively, P < 0.05). Experiment 2 showed that adipic acid supplementation reduced ammonia emission by 25% (P < 0.05), which corresponded to the predicted reduction in ammonia emission based on the reduction in manure pH observed. In conclusion, feeding adipic acid lowers urinary pH and reduces ammonia emission. The reduction in ammonia emission, though, does not correspond to the reduction in urinary pH but corresponds to the reduction in fecal pH as a result of mixing the urine and feces, in which feces act as a strong buffer.

Acid-Base Equilibrium↗
PubMed2005

Influence of dietary crude protein concentration and source on potential ammonia emissions from beef cattle manure.

Emissions of ammonia, as well as other gases and particulates, to the atmosphere are a growing concern of livestock producers, the general public, and regulators. The concentration and ruminal degradability of CP in beef cattle diets may affect urinary and fecal excretion of N and thus may affect ammonia emissions from beef cattle feed yards. To determine the effects of dietary CP concentration and degradability on potential ammonia emissions, 54 steers were randomly assigned to nine dietary treatments in a 3 x 3 factorial arrangement of treatments. Treatments consisted of three dietary CP concentrations (11.5, 13, and 14.5%) and three supplemental urea:cottonseed meal ratios (100:0, 50:50, and 0:100 of supplemental N). Steers were confined to tie stalls, and feces and urine excreted were collected and frozen after approximately 30, 75, and 120 d on feed. One percent of daily urine and feces excretion were added to polyethylene chambers containing 1,550 g of soil. Chambers were sealed, and ammonia emissions were trapped in an acid solution for 7 d using a vacuum system. As the protein concentration in the diet increased from 11.5 to 13%, in vitro daily ammonia emissions increased (P < 0.01) 60 to 200%, due primarily to increased urinary N excretion. As days on feed increased, in vitro ammonia emissions also increased (P < 0.01). Potential ammonia losses were highly correlated (P < 0.01) to urinary N (r2 = 0.69), urinary urea-N (r2 = 0.58) excretion, serum urea-N concentration (r2 = 0.52), and intake of degradable protein N (r2 = 0.23). Although dietary composition can affect daily ammonia losses, daily ammonia emissions must be balanced with effects on animal performance to determine optimal protein concentrations and forms in the diet.

Ammonia↗
PubMed1980

Influence of time after ensiling on distribution of nitrogen in corn silage treated with ammonia.

Chopped whole corn plant was treated before ensiling with 1.4% ammonia (of dry matter) to which .36% atom excess of 15N had been added. About 50 kg of material (14 kg dry matter) were placed in .5-mm polyethylene bags (of double thickness) which were evacuated and served as experimental silos. Silage samples were taken on days 0, 3, 7, 14, 21 and 50 and analyzed for N fractions. The 15N content of these fractions was analyzed by a mass spectrophotometer. N fractions of untreated silage were also determined. Between days 0 and 7 of fermentation, ammonia N decreased from 50 to 39% of the total silage N, with a corresponding increase in nonammonia N, from 50 to 60%. Thereafter, little change was noted in these fractions. Approximately 40% of the increase in non-ammonia N was in the soluble portion and 60% was in the insoluble portion. Insoluble N of treated silage was 50% higher than that of control silage. Initially, 89% of the N from added ammonia was recovered as ammonia, but this proportion decreased to 68% by day 7 and changed little thereafter. There was immediate incorporation of 43% of the ammonia into the insoluble N fraction. Most of the initial binding was as intact ammonia, with a subsequent release during fermentation. Because direct ammonia incorporation accounted for a higher percentage of the insoluble N increase on day 0 than on subsequent days, these data support earlier studies which showed that ammonia decreased breakdown of protein of the ensiled corn plant.

Ammonia↗
PubMed1996

Ammonia and glutamine metabolism during liver insufficiency: the role of kidney and brain in interorgan nitrogen exchange.

BACKGROUND: During liver failure, urea synthesis capacity is impaired. In this situation the most important alternative pathway for ammonia detoxification is the formation of glutamine from ammonia and glutamate. Information is lacking about the quantitative and qualitative role of kidney and brain in ammonia detoxification during liver failure. METHODS: This review is based on own experiments considered against literature data. RESULTS AND CONCLUSIONS: Brain detoxifies ammonia during liver failure by ammonia uptake from the blood, glutamine synthesis and subsequent glutamine release into the blood. Although quantitatively unimportant, this may be qualitatively important, because it may influence metabolic and/or neurotransmitter glutamate concentrations. The kidney plays an important role in adaptation to hyperammonaemia by reversing the ratio of ammonia excreted in the urine versus ammonia released into the blood from 0.5 to 2. Thus, the kidney changes into an organ that netto removes ammonia from the body as opposed to the normal situation in which it adds ammonia to the body pools.

Ammonia↗
PubMed2000

Microbial populations, fermentation end-products, and aerobic stability of corn silage treated with ammonia or a propionic acid-based preservative.

We studied the effects of ammonia treatment on microbial populations during the fermentation of corn silage. We also compared the effects of ammonia to a preservative containing buffered propionic acid and other antifungal compounds on the fermentation and aerobic stability of corn silage. In the first experiment, whole-plant corn was ensiled without treatment or treated with ammonia-N to supply an additional 0.3% N (fresh-forage basis). The addition of ammonia immediately increased silage pH and had no effect on numbers of lactic acid bacteria, but delayed their growth compared with untreated silage. Numbers of enterobacteria declined more slowly, but numbers of yeasts and molds declined more quickly in silage treated with ammonia. During the early stages of ensiling, lactic acid increased more rapidly in untreated than in treated silage. The reverse was true for acetic acid concentrations. When exposed to air, growth of yeasts and molds was delayed in ammonia-treated silage. In a second experiment, various levels (0.1 to 0.3%, fresh weight) of ammonium-N or a preservative with buffered propionic acid were added to whole-plant corn and allowed to ensile for 106 d. Silage treated with ammonia had a greater ratio of L- to D-lactic acid than did other silages. Untreated silage was aerobically stable for 32.3 h, whereas the low (42 h) and moderate (52.7 h) concentrations of both additives numerically improved aerobic stability. High concentrations of ammonia-N (0.3%) or a buffered propionic acid preservative (0.3%), markedly improved the aerobic stability of corn silage (82 and 69 h for ammonia and propionic acid-treated silage, respectively).

Ammonia↗
PubMed2004

Correlations among gastric juice pH and ammonia, Helicobacter pylori infection and gastric mucosal histology.

BACKGROUND: To assess the relationships among gastric pH and ammonia level, H. pylori infection, and gastric mucosal histology, we determined the gastric juice pH and ammonia concentration in H. pylori gastritis. METHODS: The pH levels and ammonia concentrations were determined in gastric juice collected from 143 patients with dyspepsia during an endoscopy and compared according to a H. pylori infection. We also looked for correlations between two chemical parameters, between each of these parameters and H. pylori density, and histology. RESULTS: Gastric pH levels and ammonia concentrations were higher in 94 infected patients than in the uninfected (3.16 vs. 1.55, p = 0.0001; 5.58 +/- 2.69 vs. 2.00 +/- 1.49 mol/L, p = 0.0001). Among 28 patients who received eradication therapy, 19 (67.9%) were successful, and their gastric pH levels and ammonia concentrations were significantly lower than those in the eradication failure group (1.60 vs. 2.33, p = 0.007; 1.77 +/- 1.28 vs. 4.02 +/- 1.20 micromoL/L, p = 0.0001). Gastric pH was significantly associated with intragastric ammonia concentration (p = 0.025) and gastritis activity (p = 0.018). Gastric pH and the ammonia level were significantly correlated with each other (rs = 0.495, p < 0.01), and with H. pylori density (rs = 0.467; rs = 0.735, p < 0.01), gastritis severity (rs = 0.343; rs = 0.478, p < 0.01), and gastritis activity (rs=0.418; rs = 0.579, p < 0.01). CONCLUSION: Gastric juice pH and ammonia concentration reflect well the status of a H. pylori infection, and significantly correlate with each other and with H. pylori density, gastritis severity and activity. These findings suggest that intragastric ammonia produced by H. pylori may have a partial role in an increased gastric juice pH, and has a pathogenic role in H. pylori gastritis.

Adult↗
PubMed2004

Acute respiratory effects of exposure to ammonia on healthy persons.

OBJECTIVES: This study investigated the acute respiratory effects of low ammonia exposure on healthy persons. METHODS: Twelve healthy persons underwent sham or ammonia (5 and 25 ppm) exposure randomly in an exposure chamber on three occasions. The exposure duration was 3 hours, 1.5 hours resting (seated) and 1.5 hours exercising (50 W on a bicycle ergonometer). Symptoms were registered repeatedly before, during, and after the exposure on visual analogue scales. Bronchial responsiveness to methacholine, lung function, and exhaled nitric oxide (NO) were measured before and 7 hours after the exposure. In addition, nasal lavage was performed, and peripheral blood samples were drawn before and 7 hours after the exposure. RESULTS: All the symptom ratings increased significantly during 25-ppm ammonia exposure as compared with the control exposure. The cumulative dose of methacholine causing a 20% decrease in forced expiratory volume in 1 second was lower (<1 concentration step of methacholine) for the exposure than for a pretrial control challenge. However, no difference was found between the control and ammonia exposures (P=0.33). The ammonia exposure did not significantly influence lung function or the exhaled NO levels. The total cell or interleukin-8 concentration in nasal lavage fluid did not change. The total leucocyte concentration in peripheral blood increased significantly (P<0.001) after both the sham and ammonia exposure, mainly due to an increase in neutrophils (P<0.001). Ammonia exposure did not significantly alter complement factor 3b in plasma. CONCLUSIONS: During ammonia exposure in an exposure chamber, symptoms related to irritation and central nervous effects increase and are constant with no signs of adaptation. Ammonia inhalation does not cause detectable upper-airway inflammation or increased bronchial responsiveness to methacholine in healthy persons.

Adult↗