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PubMed1987

Urea and glucose formation in ovine liver after ammonia and lactate loading in vivo.

Ammonium chloride (30 mumol/min/kg bw), lactate (50 mumol/min/kg bw) or ammonium chloride plus lactate were infused for two hours into the mesenteric vein of sheep. Blood samples were taken before, during, and two hours after infusion from portal, hepatic and jugular veins for estimation of ammonia, urea, lactate and glucose. Average portal and hepatic blood flow was 59 +/- 35 and 89 +/- 48 ml/min/kg bw respectively without any regular changes when ammonium chloride or lactate alone were administered. The treatment with ammonium chloride increased the hepatic ammonia fixation from 9.1 +/- 2.1 to 25.2 +/- 5.7 mumol/min/kg bw and urea formation from 17.6 +/- 14.2 to 56.4 +/- 43.2 mumol/min/kg bw. The infusion of ammonium chloride alone provoked a peripheral hyperammonaemia and it increased the endogenous sources of ammonia for urea production. Both lactate and ammonia caused an increase of hepatic glucose release. It was suggested that lactate stimulated mainly gluconeogenesis, and ammonium-glucogenolysis. The effect of ammonia in the last reaction as well as an increased net urea formation in the liver, was probably mediated by the hypoinsulinaemia and/or an increase of adrenaline secretion.

Ammonia↗
PubMed1997

Efficacy of vancomycin/tri-iododecyclemethyl ammonium chloride-coated ventriculostomy catheters in reducing infection.

OBJECTIVE: The biotoxicity of tri-iododecyclemethyl ammonium chloride (TDMAC)-coated catheters in the brain was tested, as was the efficacy of the vancomycin-bonded, TDMAC-coated catheters to inhibit staphylococcal growth in vitro and to delay the onset of clinical manifestations of catheter-related staphylococcal ventriculitis in rabbit experimental model. METHODS: The brain toxicity of the TDMAC-coated catheters was tested in New Zealand White rabbits. The efficacy of the vancomycin-bonded, TDMAC-coated catheters in the inhibition of staphylococcal growth was tested in agar seeded with Staphylococcus aureus and Staphylococcus epidermidis strains. Sections of vancomycin-bonded, TDMAC-coated catheters were placed in saline solution for testing of drug release over time. Stereotactic placement of ventriculostomy catheters was performed in two groups of New Zealand White rabbits. In the experimental group, vancomycin-bonded, TDMAC-coated catheters were used. In the control group, TDMAC-coated catheters were used. Staphylococcal colonies were inoculated at the exit site of the catheters. Culture of the catheter tips was performed at the time of death of the animals. RESULTS: No toxic reactions were seen at the implantation sites or in surrounding brain. Significant inhibition of growth of both S. aureus and S. epidermidis was noted with the vancomycin-bonded catheters (P = 0.01). Vancomycin continued to be released from catheters for the full 6 days of the study. The median interval to development of clinical manifestations of ventriculitis among the experimental group of rabbits was 53 days; among the control group, the interval was 27 days (P < 0.001). CONCLUSION: Vancomycin-bonded, TDMAC-coated ventriculostomy catheters bind and release the drug at levels exceeding the minimum inhibitory concentration for S. aureus and S. epidermidis for at least 6 days and can significantly delay the onset of infectious ventriculitis in a rabbit model.

Animals↗
PubMed1985

Modification of interactions between neutrophils and staphylococci by lysosomotropic weak bases.

Weak bases that alkalinize the pH within neutrophil lysosomes inhibit in vitro cell functions, including lysosomal enzyme release and superoxide production. To determine the relevance of this inhibition to microbicidal activity, the effect of lysosomotropic weak bases on interactions between human neutrophils and Staphylococcus aureus 502a was studied. After treatment with 1 mM chloroquine, neutrophils showed significantly impaired phagocytosis of 14C-labeled S. aureus. However, 50 mM ammonium chloride had no effect on phagocytosis, although we have previously shown that this concentration raises lysosomal pH and inhibits degranulation and superoxide production. This base was therefore used to study effects on intracellular microbicidal activity. Incubation of neutrophils with 50 mM ammonium chloride diminished killing of S. aureus (22.9 +/- 6.3% of bacteria surviving versus 8.2 +/- 1.3% in suspensions without ammonium chloride). At 1 mM, ammonium chloride had no significant effect. The inhibition of cellular function could be neither explained as a function of neutrophil death, as measured by trypan blue dye exclusion, nor attributed to direct promotion of bacterial growth (in the absence of neutrophils, colony counts were similar in the presence or absence of ammonium chloride) or enhanced resistance to neutrophil microbicidal mechanisms (bacteria treated with ammonium chloride and washed before neutrophil exposure showed no improvement in survival). Ammonium chloride at 50 mM also impaired neutrophil killing of S. aureus in an anaerobic chamber, but microbicidal activity against Escherichia coli S15 was not affected. These findings suggest that optimal neutrophil killing of staphylococci requires a highly acid intralysosomal compartment, but ingestion of bacteria does not. This may reflect primary failure of acidification of the phagocytic vacuole or differential pH requirements for fusion of the plasma membrane with itself and with lysosome membranes. The difference between effects on killing of S. aureus and E. coli is probably a result of the relative importance of the components of neutrophil microbicidal activity against the two organisms.

Ammonium Chloride↗
PubMed1999

Effects of ammonium chloride-induced acidosis on oxidative metabolism in liver mitochondria of chicks.

The present studies were undertaken to characterise oxidative metabolism with diverse substrates in hepatic mitochondria of acidotic chicks. Metabolic acidosis was experimentally induced by replacement of drinking water with ammonium chloride solution (15 g/l) for 5 d. State 3 oxidation rates in liver mitochondria were significantly reduced in acidotic chicks only for pyruvate and glutamate as substrates requiring complex I, III and IV of the electron transport chain, while they were not changed for either succinate-requiring complexes II, III and IV, ascorbate+TMPD-requiring complex IV, or alpha-ketoglutarate requiring complexes I, III and IV. It can be concluded that the impairment of oxidation rate was substrate-specific in liver mitochondria of acidotic animals and not associated with functional damage of the respiratory chain in mitochondria. Possible reasons for the reductions in oxidation rate with pyruvate and glutamate are discussed.

Acidosis↗
PubMed2002

Ammonium chloride-promoted four-component synthesis of pyrrolo[3,4-b]pyridin-5-one.

A novel multicomponent synthesis of 5-aminooxazole starting from simple and readily available inputs is described. Thus, simply heating a methanol solution of an aldehyde 3, an amine 4, and an alpha-isocyanoacetamide 5 provided the 5-aminooxazole (1) in good to excellent yield. The reaction of 1 with alpha,beta-unsaturated acyl chloride 13 lead to the formation of pyrrolo[3,4-b]pyridin-5-one (2) in a single operation. A triple domino sequence, acylation/IMDA/retro-Michael cycloreversion, is involved in this new scaffold-generating reaction. After the observation that ammonium chloride can significantly accelerate the oxazole formation in toluene, a one-pot four-component synthesis of 2 is developed.

Ammonium Chloride↗
PubMed1992

Ammonium chloride-induced acidosis increases protein breakdown and amino acid oxidation in humans.

The effect of acidosis on whole body protein turnover was determined from the kinetics of infused L-[1-13C]leucine. Seven healthy subjects were studied before (basal) and after (acid) the induction of acidosis with 5 days oral ammonium chloride (basal pH 7.42 +/- 0.01, acid pH 7.35 +/- 0.03). Bicarbonate recovery, measured from the kinetics of infused NaH13CO3, was increased in the acidotic state (basal 72.9 +/- 1.2 vs. acid 77.6 +/- 1.6%; P = 0.06). Leucine appearance from body protein (PD), leucine disappearance into body protein (PS), and leucine oxidation (O) increased significantly (PD: basal 120.5 +/- 5.6 vs. acid 153.9 +/- 6.2, P < 0.01; PS: basal 98.8 +/- 5.6 vs. acid 127.0 +/- 4.7, P < 0.01; O: basal 21.6 +/- 1.1 vs. acid 26.9 +/- 2.3 mumol.kg-1.h-1, P < 0.01). Plasma levels of the amino acids threonine, serine, asparagine, citrulline, valine, leucine, ornithine, lysine, histidine, arginine, and hydroxyproline increased significantly with the induction of acidosis. These results confirm that acidosis in humans is a catabolic factor stimulating protein degradation and amino acid oxidation.

Acidosis↗
PubMed1982

Monensin blocks the transport of diphtheria toxin to the cell cytoplasm.

Lysosomotropic amines are believed to inhibit the transport of diphtheria toxin to the cell cytoplasm by raising the pH within intracellular vesicles. If so, then other drugs that dissipate intracellular proton gradients should have a similar effect on toxin transport. We found that monensin, a proton ionophore unrelated to lysosomotropic amines, is a potent inhibitor of the cytotoxic effect of diphtheria toxin. Monensin appears to block the escape of endocytosed toxin from a vesicle to the cytoplasm. Monensin fails to protect cells from the effects of diphtheria toxin that is bound to the cell surface and exposed to acidic medium, suggesting that the step normally blocked by the drug is circumvented under these conditions. The inhibition of toxin transport caused by monensin could not be relieved when monensin was replaced by ammonium chloride, nor when ammonium chloride was again replaced by monensin. This suggests that both drugs block the same step of toxin transport. The effect of monensin on the transport of diphtheria toxin to the cytoplasm is consistent with the proposal (Draper and Simon. 1980. J. Cell Biol. 87:849-854; Sandvig and Olsnes. 1980. J. Cell Biol. 87:828-832) that the toxin is endocytosed and then, in response to an acidic environment, penetrates through the membrane of an intracellular vesicle to reach the cytoplasm.

Animals↗
PubMed1984

Urinary acidification in the prevention and treatment of feline struvite urolithiasis.

Two groups of 12 cats were fed ad libitum an experimental dry expanded ration high in magnesium (0.37%, dry matter basis) and similar to most commercial dry cat foods in all other nutrients. The diet of one of the groups contained 1.5% ammonium chloride, which was added to the diet before processing. Urethral obstruction developed twice in 7 of the 12 cats fed the ration without ammonium chloride. Of the 5 remaining cats in that group, 2 had calculi in the urinary bladder and urethra at necropsy. In contrast, only 2 of the 12 cats fed the ration containing ammonium chloride had urethral blockage once; neither cat had another blockage. Both cats had been catheterized twice as paired controls before urethral obstruction. One of these 2 cats died from a urinary tract infection apparently introduced through the indwelling catheter, and at necropsy there were 2 small calculi in the urethra. At the end of the study, only 1 other cat fed the ammonium chloride diet had a calculus in the urinary bladder at necropsy; this cat had not had a urethral obstruction throughout the study. After each cat had 2 urethral blockages, its diet was changed. Four cats were fed the ration containing ammonium chloride and 3, a dry, commercial ration. Of the 4 cats fed the diet containing ammonium chloride, none developed another urethral obstruction within 6 months, and at necropsy, no calculi were in the urinary bladder or urethra. Two of the 3 cats fed the commercial ration experienced urethral blockage within 3 months. These 2 cats were then fed the diet containing ammonium chloride.(ABSTRACT TRUNCATED AT 250 WORDS)

Ammonium Chloride↗
PubMed1975

Chemical modulation of diphtheria toxin action on cultured mammalian cells.

Ammonium chloride (4 times 10-3 M) rendered HEp-2 monolayers completely insensitive to the action of diphtheria toxin, as measured by de novo protein synthesis. Total protection was observed even with large amounts of toxin (400 minimum lethal doses/ml). Ammonium chloride did not reduce toxicity by direct action on the protein, nor did it prevent the adsorption of toxin to the cell membrane. Although the ammonium salt did not block the initial interaction between cell and toxin, it did maintain the toxin at a site amenable to neutralization with antitoxin. Surface-adsorbed toxin was inactivated by cellular enzymes or alternatively was desorbed from the membrane during a 12-h incubation in the presence of ammonium chloride. In addition, ammonium chloride provided protection to both toxin-sensitive guinea pig peritoneal macrophages and a partially toxin-resistant strain of HEp-2 cells. Sodium arsenite was effective in protecting cell monolayers from the action of diphtheria toxin; unlike ammonium chloride, its action was not dependent upon continued incubation with cells during exposure to toxin. Inhibitors of energy metabolism abolished toxin action either totally (sodium fluoride) or partially (dinitrophenol and sodium cyanide). Inhibitors of cellular proteases, on the other hand, did not modify toxin activity. The ability of several modifiers of membrane function to alter expression of toxicity for HEp-2 cells was also examined. One compound known to enhance endocytic activity, Tuftsin, had no effect, whereas poly-L-ornithine provided partial protection. Of the two compounds known to alter membrane fluidity, cytochalasin B provided partial protection for HEp-2 cell cultures, whereas colchicine had no effect. Agents that bind to sulfhydryl groups on the cell surface had no apparent effect on toxicity, suggesting that the initial toxin-cell interaction does not involve sulfhydryl groups. Those compounds that provide virtually full protection against the action of diphtheria toxic on cell monolayers (i.e., ammonium chloride, sodium fluoride, and sodium arsenite) had no inhibitory effect on the in vitro enzyme activity associated with fragment A of the toxin.

Ammonium Chloride↗
PubMed1989

Effects of dibutyryl cyclic AMP on hemodynamics and plasma catecholamine concentrations during ammonium chloride-induced metabolic acidosis in anesthetized dogs.

We investigated, using anesthetized dogs, the effect of dibutyryl cyclic AMP (db-cAMP), a derivative of cyclic AMP (cAMP), on cardiovascular variants and plasma catecholamines during metabolic acidosis. These effects were also compared with those of dopamine. The db-cAMP and dopamine were infused at 200 and 20 micrograms/kg.min, respectively. Metabolic acidosis (pH 7.00, PaCO2 40 torr) was induced by the iv infusion of 1-M ammonium chloride solution (NH4Cl). In the normal acid-base state, both db-cAMP and dopamine significantly increased cardiac output and decreased systemic vascular resistance (SVR). During metabolic acidosis, db-cAMP increased cardiac output by 69 +/- 14% and decreased SVR by 36 +/- 2%, while dopamine did not produce changes in cardiac output and increased SVR. Dopamine caused an elevation of epinephrine and norepinephrine in the normal acid-base state, but db-cAMP did not. During metabolic acidosis, dopamine significantly increased the plasma concentration of epinephrine and norepinephrine, while db-cAMP significantly decreased epinephrine concentration. These results suggest that db-cAMP may have a more beneficial effect on hemodynamics compared with dopamine when therapeutic support is needed during circulatory insufficiency with severe metabolic acidosis.

Acidosis↗
PubMed1980

Effect of NH4Cl on phosphaturic response to PTH in the hamster: dissociation from acidemia.

Previous studies indicate that the hamster fasted for 16 h fails to demonstrate a significant phosphaturic response to parathyroid hormone (PTH). However, when hamsters were infused with ammonium chloride, a phosphaturic response to PTH was observed. The present studies evaluate the respective roles of acidemia and the ammonium ion in this response. As in previous studies, fasted thyroparathyroidectomized (TPTX) hamsters infused with PTH showed no significant increase in the fractional excretion of phosphate (FE rho), from 19 +/- 2 to 22 +/- 1%. Neither respiratory acidosis (hypercapnia) nor metabolic acidosis (HCl infusion) enhanced the phosphaturic effect of PTH, FE rho 21 +/- 4 to 20 +/- 6 and 15 +/- 2 to 16 +/- 3%, respectively. Both ammonium chloride and ammonium bicarbonate infusions enhanced the phosphaturic response; FE rho increased from 15 +/- 5 to 27 +/- 5% (P < 0.02) and 17 +/- 3 to 25 +/- 3% (P < 0.05), respectively. We conclude that the enhancement of the phosphaturic effect of PTH in the fasted hamster by ammonium chloride infusions can be dissociated from acidemia.

Acidosis↗
PubMed1980

[Urea synthesis in the myocardium].

Urea synthesis was studied in the isolated rat heart-perfused with ammonium chloride (10 mM), mixtures of ammonium chloride (10 mM) and 1-aspartic acid (10 mM), 1-ornithine (2.5 mM), 1-arginine (10mM), 1-glutamine (10 mM), 1-alanine (10 mM), 1-leucine (5 mM) and pyruvate (5mM). Ammonium chloride and 1-arginine are the most effective activators of urea synthesis, while 1-leucine and pyruvate produce an inhibitory action. The possibility of ammonia hinding in heart tissue was shown by means of (15)N. The amount of urea incorporated (15)N grows as the concentration of (15)N-ammonium in the perfusate increases from 1.6 to 3.4 mM. Isoproterenol-induced necrosis of the heart muscle leads to a significant increase in the urea incorporated (15)N.

Amino Acids↗
PubMed1975

Adaptations in urea ammonium excretion in metabolic acidosis in the rat: a reinterpretation.

1. The effects of oral hydrochloric acid, ammonium chloride, sodium bicarbonate and ammonium bicarbonate on urea and ammonium excretion in rats on a constant diet were studied. 2. Hydrochloric acid acidosis significantly reduced urea excretion in the rat, with an equimolar increase in NH+4 excretion and no change in their sum. In ammonium chloride acidosis, most of the additional nitrogen intake is excreted as NH+4 and a small percentage as urea. The converse holds true after administration of ammonium bicarbonate. The physiological significance of this is discussed. 3. The shift in nitrogen excretion from urea to NH+4 in acidosis is interpreted on the basis of bicarbonate production and utilization. Urea formation utilizes HCO-3. For amino acid sources, this utilization is offset by the metabolism of the carbon skeleton, which gives rise to HCO-3. When waste nitrogen is excreted as NH+4, no bicarbonate is utilized and the new HCO-3, generated by the carbon skeleton, hels to maintain hydrogen ion homeostasis.

Acidosis↗
PubMed1986

Mechanisms of pH regulation in lamprey (Lampetra fluviatilis) red blood cells.

Mechanisms regulating the red cell pH in lamprey (Lampetra fluviatilis) were studied using the ammonium chloride prepulse technique. The cells were initially incubated in a physiological saline containing 20 mmol l-1 ammonium chloride, and intracellular pH measured with the DMO technique. Ammonium chloride was then rapidly removed by centrifugation, and the changes in the intracellular pH followed. The intraerythrocytic pH is primarily regulated by an amiloride-sensitive sodium/proton exchange. When sodium is present in the incubation medium, the intracellular pH rapidly recovers from the acidification associated with the removal of ammonium chloride from the incubation. When sodium is removed from the incubation medium, intracellular pH does not recover, and when the cells are treated with 10(-3) mol l-1 amiloride in the presence of sodium, carbon dioxide and bicarbonate, the intracellular pH recovery is drastically reduced. The movements of carbon dioxide, its consecutive catalysed hydration and dissociation to protons and bicarbonate and, possibly, movements of bicarbonate out of the cell acidify the cell contents. This is shown by the observation that the steady-state intracellular pH is higher in a HEPES-buffered medium than in a CO2/HCO3(-)-buffered medium at the same extracellular pH. The acidification is dependent on cellular carbonic anhydrase activity, present in lamprey red cells, which speeds up the hydration reaction. When the action of carbonic anhydrase is inhibited by acetazolamide, removal of ammonium chloride from the incubation medium does not cause intracellular acidification.

Ammonium Chloride↗
PubMed1986

The effect of antibody valency and lysosomotropic amines on the synergy between ricin A chain- and ricin B chain-containing immunotoxins.

The cytotoxicity of A chain immunotoxins containing IgG or Fab fragments specific for the surface immunoglobulin of the Daudi cell line was assessed in the presence of B chain immunotoxins (IgG or Fab) or lysosomotropic amines, or both. The concentration required for 50% inhibition of protein synthesis (IC50) in Daudi cells was 1.3 X 10(-8) M for IgG-A and 5 X 10(-8) M for Fab-A. The toxicity of both A chain immunotoxins was enhanced twofold by ammonium chloride. In the presence of A chain immunotoxins and ammonium chloride, a maximum of 99 and 90% reduction of clonal precursors was obtained with IgG and Fab-A chain immunotoxins respectively. Immunotoxins containing ricin B chain and IgG or Fab fragments specific for the antibody portion of A chain immunotoxins were used as secondary "piggyback" immunotoxins to treat cells that were pretreated with A chain immunotoxins. Both B chain immunotoxins were nontoxic at 1 X 10(-6) M. When added to target cells pretreated with specific A chain immunotoxins, the IC50 of the A chain immunotoxins was decreased up to 16-fold in the absence of ammonium chloride. In contrast to the results obtained with A chain immunotoxins alone, ammonium chloride significantly increased the toxicity of the complete piggyback system, resulting in the killing of 99.999% or five logs of target cells in the clonal assay. This decreased the IC50 of A chain immunotoxins up to 116-fold when compared with A chain immunotoxin alone. This enhanced toxicity was independent of the valency of either immunotoxin.

Adjuvants, Immunologic↗
PubMed1984

Effect of ammonium on bacterial adherence to bladder transitional epithelium.

The virulence of urease-producing bacteria depends on the ability of urease to degrade urea into ammonia and thereby to alkalinize the urine. Infections caused by urease-producing organisms such as Proteus mirabilis are particularly difficult to manage clinically. We have shown that the layer of glycosaminoglycans at the bladder surface protects against infection by blocking the adherence of bacteria to the epithelium. To determine whether urease-producing urinary pathogens owe their virulence in part to an ability to inactivate the protective effect of the glycosaminoglycan layer, we tested the ability of ammonium chloride to alter bacterial adherence to the normal vesical mucosa. We used an in vivo adherence assay that we have described previously in rabbits. Control animals received sodium chloride adjusted to the same pH as the ammonium chloride. We found that 0.25 M ammonium chloride significantly increases bacterial adherence to normal vesical mucosa as compared to adherence in controls receiving 0.25 M sodium chloride (p less than 0.05). These data suggest that urease plays a hitherto undescribed role in bacterial virulence by altering the antiadherence activity of the glycosaminoglycan layer present at the transitional cell surface.

Adhesiveness↗
PubMed1972

Effect of Transpiration-reducing Chemicals on Growth, Flowering, and Stomatal Opening of Tomato Plants.

Phenyl mercuric acetate, 8-hydroxyquinoline, N-dimethylamino succinamic acid, or 2-chloroethyl trimethyl ammonium chloride were sprayed on 37-day-old tomato (Lycopersicon esculentum Mill. cv. Sioux) plants seven times at weekly intervals. Plants of nearly normal appearance resulted with all treatments except 2-chloroethyl trimethyl ammonium chloride. There was no change in leaf number, but 2-chloroethyl trimethyl ammonium chloride increased the number of flowers. 2-Chloroethyl trimethyl ammonium chloride and phenyl mercuric acetate caused earlier flowering. Yield was not affected significantly. Stomatal opening was reduced 80% immediately after spraying with phenyl mercuric acetate or 2-chloroethyl trimethyl ammonium chloride, but 6 days after spraying, the reduction in stomatal opening was only 30 to 40%. Wilting was delayed 8 days by phenyl mercuric acetate and 4 days by 2-chloroethyl trimethyl ammonium chloride and N-dimethyl amino succinamic acid treatments, when water was withheld 59 days after the final spray application.

Journal Article↗