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PubMed1978

[Acid-excreting activity of the kidneys in dogs administered ammonium chloride into the carotid artery].

Injection of 0.5 mM of ammonium chloride into the dog carotid artery caused no changes in the blood acid-base balance, but distinctly increased the urinary excretion of both titratable acids and active hydrogen ions. The rate of glomerular filtration was slightly increased. The amount of sodium reabsorbed in the tubules was also risen. The role of humoral factors stimulating the renal acid-excreting activity, is discussed.

Acid-Base Equilibrium↗
PubMed1986

Use of ammonium chloride and sodium bicarbonate in acute heat exposure of broilers.

Ammonium chloride (NH4Cl) and sodium bicarbonate (NaHCO3) were added separately to the drinking water of 42- to 52-day-old broilers. Birds were given access to the water ad libitum for a total of 42.5 hr consisting of 18.5 hr prior to an 8-hr interval of severe heat exposure and a further 16 hr-post exposure. Water and feed intake during the treatment period were unaffected by either NH4Cl at 6.25 g/liter (.63%) of distilled water (DW) or NaHCO3 at 3.15 g/liter (.32%) DW. Water intake was increased by approximately 20% in birds given water containing 6.25 g of NaHCO3/liter (.63%) DW, while both feed and water intake were severely limited by NH4Cl at 31 g/liter (3.1%) DW. Blood pH of birds was substantially lowered by consumption of NH4Cl, while consumption of NaHCO3 did not significantly affect blood pH. Blood pH of all treatments increased during the heat exposure period and declined afterward; however, blood pH change appeared to be more pronounced for birds receiving the NH4CL. A correlation coefficient (r = -.31) existed between blood pH and mortality, while a correlation (r = -.72) was demonstrated between water consumption and mortality.

Ammonium Chloride↗
PubMed1991

Kinetic analysis of the preserved rat liver by isolated perfusion with ammonium chloride as a load.

Oxygen consumption and urea synthesis from ammonium chloride (NH4Cl) were investigated in the liver preserved in University of Wisconsin solution at 4 degrees C for 24 hours using an isolated rat liver perfusion system in which the perfusate contained five different concentrations of NH4Cl. When a Michaelis-Menten equation was applied to oxygen consumption and urea synthesis against NH4Cl concentration, the preserved liver showed smaller increase in oxygen consumption rate and larger Km of urea synthesis for NH4Cl than the fresh liver. The ratio of respiration velocity without any substrate to maximal velocity (v/Vmax), which reflects the mitochondrial functional reserve, was 55.9 +/- 4.1% and 41.5 +/- 4.8% in the preserved and fresh liver, respectively (p less than 0.05). From the viewpoint of work-cost relationship, it was shown that the mitochondrial function in the preserved liver was deteriorated. On the other hand, conventional mitochondrial study after rewarming and reoxygenation but before NH4Cl load revealed no deterioration of mitochondrial function after preservation. These results indicate that it is necessary to take the metabolic load on the reperfused liver into account when assessing graft viability, and that high v/Vmax suggests decrease in the reserve of mitochondrial function under consideration of the metabolic load.

Ammonium Chloride↗
PubMed1998

Influence of ammonium chloride on the tissue distribution of anticholinergic drugs in rats.

Ammonium chloride (NH4Cl) increases lysosomal pH and thereby abolishes intralysosomal accumulation of drugs. Its effect on the tissue distribution of biperiden and trihexyphenidyl in rats has been investigated. The tissue-plasma concentration ratios (Kp) of these drugs in various tissues were determined by infusion studies at steady-state in the presence or absence of NH4Cl. Treatment with NH4Cl reduced the Kp values for both drugs, causing the largest reduction in Kp in the lung (52.1 to 11.8 for biperiden and 59.5 to 18.9 for trihexyphenidyl; ratios of decrease 0.77 and 0.68, respectively), followed by the heart and kidneys, with relatively small reductions in the brain, gut, muscle and fat. Subcellular fractionation studies in the lung indicated that the subcellular fraction-plasma concentration ratio of each drug at the steady state (K(p,sf)) was reduced by treatment with NH4Cl, with the largest decrease in the post-nuclear fraction (ratio of decrease 0.82 for biperiden and 0.74 for trihexyphenidyl), followed by the nucleus, microsomes and supernatant, in that order. A strong correlation was found between the ratio of decrease in K(p,sf) after NH4Cl treatment and the specific activity of acid phosphatases, a marker of lysosomes, in each fraction (biperiden, r = 0.948; trihexyphenidyl, r = 0.945). These results suggest that acidic organelles contribute significantly to the distribution kinetics of anticholinergic drugs.

Adipose Tissue↗
PubMed1994

Bone marrow transplantation demonstrates that carbonic anhydrase II deficiency limited to bone marrow-derived cells affects ammonium chloride tolerance in mice.

Bone marrow transplantation (BMT) in mice was utilized to determine the relative importance of carbonic anhydrase II (CA II) deficiency in blood compared to kidney in the pathogenesis of the ammonium chloride intolerance observed in CA II-deficient mice. "Normal" BMT experiments utilized normal donors and CA II-deficient recipients (NL-->DEF), "reverse" BMT experiments utilized CA II-deficient donors and normal recipients, and control BMT experiments utilized normal mice with a hemoglobin polymorphism (Hbb d/s). Unstressed urinary pH was not significantly altered by normal or reverse BMT, nor was any change induced by control BMT. However, DEF-->NL mice showed markedly altered weight changes when placed on oral ammonium chloride, an effect apparently secondary to dehydration due to decreased water intake. In addition, some CA II-deficient mice have a urinary concentrating defect. Red blood cell and kidney CA II deficiency contribute additively to these effects.

Ammonium Chloride↗
PubMed1993

[The effect of a toxic dose of ammonium chloride on brain bioelectrical activity in rats].

A toxic dose of ammonium chloride (> 12 mmol/kg) caused death of animals within 10 min of i.p. injection, while pentobarbital--(40 mg/kg, i.p.) and kurare--(0.2 mg/kg, i.v.) injected rats died only in 11% of the tests. At 40 min after the injection of NH4Cl, the kurare-treated animals had minimum EEG amplitude in the cortex, maximum--in RF, and unchanged in amygdala. At the same time evoked potentials (EP) in RF induced by the periphery stimuli remained unchanged in form and increased in amplitude. Corticofugal impulses had no specific influence on the formation of EP in RF. The initial potentials were restored within 3 hrs. Thus, it could be concluded that ammonium differentiatively changed the state of the normal brain functional systems; it increased the afferentation and excitation of RF which could lead to violation of the vitally important functions especially breathing and cause the lethal outcome.

Ammonium Chloride↗
PubMed1997

Effect of ammonium chloride on energy metabolism of astrocytes and C6-glioma cells in vitro.

Increased ammonia has been considered a key factor in the pathogenesis of hepatic encephalopathy. The high concentration of ammonia interferes with oxidative metabolism in the brain through an inhibitory effect on the tricarboxylic acid cycle (TCA). Inhibition of the TCA cycle may result in depletion of ATP. Due to the involvement of astrocytes in brain detoxification of ammonia, these cells are good candidates for studying ammonia's effect on energy stores in the brain. C6-glioma cells, which have altered glycolytic rates, may show greater sensitivity to the toxicity of ammonium chloride than astrocytes. To study the effect of ammonium chloride on energy storage of both astrocytes and C6-glioma, we observed the acute and chronic effects of NH4Cl (7.5 or 15 mM) on the metabolism of isolated astrocytes and C6-glioma cells. Primary astrocytes were isolated from the cerebral hemispheres of 1-2 day old Sprague-Dawley rats, and C6-glioma cells were purchased from the American Type Culture Collection (ATCC). Following treatment of the cells with ammonia, glucose, lactate, glutamate, ATP, and PCr were assayed. Our data showed that at 15 min following treatment with NH4Cl, there were no significant differences in the concentration of metabolites measured in astrocytes. However, following 15 min of treatment with NH4Cl, the concentration of some metabolites, for example, ATP and lactate, changed significantly in C6-glioma cells. We have shown that 24 h of treatment was sufficient time to see significant biochemical changes but not morphological changes in either cell type. Simultaneous biochemical and morphological changes were observed 48 h following treatment in C6-glioma cells and at 9-10 days following treatment in primary astrocytes. In primary astrocytes at 24 h following treatment, glucose utilization increased. This high utilization of glucose was in accordance with the increase in lactate and glutamate production and the decrease in ATP and PCr formation. In C6-glioma cells the utilization of glucose increased but this high utilization of glucose was consistent with a significant decrease in the concentration of lactate, glutamate and ATP.

Adenosine Triphosphate↗
PubMed1987

[In vitro studies on microbial incorporation of nitrogen from [15N2] urea and [15N]ammonium chloride by human intestinal flora].

6 typical bacteria species of the human intestinal flora (E. coli, Klebsiella pneumoniae, Proteus vulgaris, Streptococcus faecalis, Bacteroides fragilis, Bifidobacterium sp.) were incubated in a liquid medium for 48 h with [15N2]-urea and [15N]-ammonium chloride. The rates of [15N]-incorporation were calculated. They depend reproducible on the species examined, on the kind of the offered NPN-substance and on the amount of NPN-substance in the medium. With [15N2]-urea the minimal rate of incorporation was 3.8% (E coli) and the maximal one 95.6% (Bifidobacterium sp.). With [15N]-ammonium chloride the corresponding figures were 31.0 (Proteus vulg.) and 98.0% (Bifidobacterium sp.). The findings are discussed with regard to a possible enteral detoxification in uremic patients by bacterial utilization and elimination of urea and ammonia.

Ammonium Chloride↗
PubMed1972

Surface-bonded antimicrobial activity of an organosilicon quaternary ammonium chloride.

The hydrolysis product of 3-(trimethoxysilyl)-propyldimethyloctadecyl ammonium chloride exhibited antimicrobial activity against a broad range of microorganisms while chemically bonded to a variety of surfaces. The chemical was not removed from surfaces by repeated washing with water, and its antimicrobial activity could not be attributed to a slow release of the chemical, but rather to the surface-bonded chemical.

Acetates↗
PubMed1974

Ammonium chloride poisoning in chronic renal disease.

A 58-year-old woman with a long history of renal stone disease and urinary tract infection presented to the emergency room with exhaustion and air hunger. Laboratory data confirmed profound metabolic acidosis. Unduly large quantities of bicarbonate and potassium were required for correction of the deficits. She had been taking 6 g daily of ammonium chloride as a urine-acidifying agent for a period of six months in addition to agents directed against urinary tract infection. The combination of impaired renal function and effective hydrogen ion loading resulted in profound systemic acidosis. The metabolic derangements associated with the administration of ammonium chloride and its use as a therapeutic agent are discussed.

Acidosis↗
PubMed1991

Ammonium chloride metabolic acidosis and the activity of renin-angiotensin-aldosterone system in children.

The present study was undertaken to assess the effects of acute metabolic acidosis on the activity of the renin-angiotensin-aldosterone system in 12 children with a mean age of 8.9 years who underwent NH4Cl loading test. Ammonium chloride was given in a dose of 0.15 g/kg per day for 3 consecutive days to evaluate renal acidification. Prior to and following NH4Cl administration blood acid-base parameters, plasma and urine electrolytes, creatinine and aldosterone concentrations as well as plasma renin activity (PRA), urine flow rate and net H+ excretion were measured. Ammonium chloride administration significantly depressed blood pH (P less than 0.05), bicarbonate (P less than 0.01) and base excess (P less than 0.01) and resulted in a slight, but significant elevation of plasma potassium concentration (P less than 0.05). Furthermore, NH4Cl ingestion induced a marked increase in urine flow rate (P less than 0.01) and urinary sodium, potassium and chloride excretion (P less than 0.01). In response to NH4Cl metabolic acidosis, PRA doubled (4.72 +/- 1.18 vs 8.13 +/- 1.02 ng/ml per hour, P less than or equal to 0.05) and there was a nearly four-fold increase in plasma aldosterone level (0.49 +/- 0.12 vs 1.52 +/- 0.24 ng/ml, P less than 0.01) and in urinary aldosterone excretion (19.2 +/- 4.3 vs 71.8 +/- 13.8 micrograms/day, P less than 0.01). The elevated aldosterone production observed in this study is assumed to be mediated by the combined effect of sodium and water diuresis-related increased PRA, hyperkalaemia and the direct stimulation of adrenal steroidogenesis by metabolic acidosis.

Acid-Base Equilibrium↗
PubMed1995

Initiation of anterior head-specific gene expression in uncommitted ectoderm of Xenopus laevis by ammonium chloride.

The role of homeobox-containing genes in the regional specification of the vertebrate embryo has been an area of intense research over the last decade. Whereas it appears that the homeobox genes of the Hox gene family play an important role in the specification of the trunk, the genes and processes involved in the specification of the head are less well understood. We have isolated a new head-specific homeobox gene, XANF-2, that appears to be involved in the regional specification of the anterior head of Xenopus embryos. This gene is initially expressed in the anterior dorsal region of early embryos and later exclusively in the primordium of the anterior pituitary gland. XANF-2 represents the earliest marker for the anterior pituitary lineage. Ammonium chloride is able to induce the expression of XANF-2 in uncommitted ectoderm. These and other data indicate that ammonium chloride is capable of inducing a large portion of the anterior dorsal region of the embryo which includes, but is not limited to, the anterior pituitary gland and cement gland anlagen. This implies that changes in intracellular ionic conditions play an important role in the formation of the anterior head region. In addition to NH4Cl, injection of follistatin RNA can induce transcription of XANF-2, suggesting that these two unrelated compounds can activate a chain of events leading to the formation of the amphibian head. Furthermore, we demonstrate that planar induction in Keller sandwiches can induce XANF-2 expression as well as the expression of the cement gland-specific gene, XCG 13, indicating that planar signaling can account for induction of even the most anterior regions of the embryo.

Amino Acid Sequence↗
PubMed2000

Reduced ammonium chloride haemolysis time enhances the number of isolated functional rabbit polymorphonuclear neutrophils.

In the present study we compared seven different methods for isolating rabbit polymorphonuclear neutrophils (PMNs) with a view to assessing viability, lymphocyte contamination and isolation yield. The two methods offering the best isolation yield and functional PMNs were retained. Leukocyte-containing plasma fraction was obtained after erythrocyte sedimentation with dextran. First, PMNs were isolated from this fraction, using hypotonic ammonium chloride haemolysis followed by Histopaque density gradient centrifugation (Method-A). Second, PMNs were obtained from leukocyte-containing plasma after centrifugation on two Percoll layers (Method-B). These processes resulted in a high cellular yield: 2.66x10(6)+/-0.22 PMNs per ml of blood (Method-A) and 1.87x10(6)+/-0.37 PMNs per ml of blood (Method-B). In both cases the PMNs isolated were of high purity and viability. In comparison, when using the standard techniques for rabbit - consisting of ammonium chloride haemolysis taking at least four times as long--fewer PMNs were isolated. The PMNs isolated by Method-A and -B were able to generate a high amount of reactive oxygen species (ROS) after stimulation with phorbol 12-myristate 13-acetate (PMA). These methods to separate PMNs are recommended for in vitro studies.

Ammonium Chloride↗
PubMedDate not supplied

[The use of urokinase and ammonium chloride in unblocking a central venous catheter in a child with acute lymphoblastic leukemia].

Central venous catheter (C.V.C.) mechanical obstruction in immunocompromised patients can yield several complications sometime life-threatening and can be promptly solved by thrombolytic treatment. The authors describe a case of a child affected by acute lymphoblastic leukemia and experiencing an obstruction of his C.V.C. very difficult to treat with conventional urokinase treatment. Thinking the lack of success to be attributed to a calcium thrombus, the Authors before pulling out the C.V.C., made use of ammonium chloride solution in order to obtain the disappearance of the little bag covering the tip of C.V.C. The treatment was successful as confirmed by the contrast medium examination and the use of C.V.C. lasted for several months without other mechanical obstruction. In our best knowledge this is one of the first attempts with such ammonium chloride solution which have been used successful and rather safely. The only drug induced symptoms were constituted by mild and transient vomiting. Owing to this positive experience the authors believe useful to confirm this treatment in other cases. In this contest an experienced hematoncology team must take care of C.V.C. related complications.

Ammonium Chloride↗
PubMedDate not supplied

Structure investigations of agonists of the natural neurotransmitter acetylcholine II [1]. X-ray structure analysis of trimethyl(4-oxopentyl)ammonium-chloride.

The crystal structure of Trimethyl(4-oxopentyl)ammonium-chloride ([(CH3)3N--(CH2)3COCH3]Cl-) (1) was determined by an X-ray structure analysis. 1 crystallizes in the orthorhombic space group P2(1)2(1)2(1) with a = 10.440 (3), b = 14.600 (9), c = 6.804 (9) A and with four formula units per unit cell. The structure was solved by a Patterson and a successive Fourier synthesis. The least squares refinement yielded an R-value of 0.064 for 1077 observed reflections. The cation of 1 is derived from acetylcholine by replacement of the ester oxygen with a CH2 group. It shows a potent nicotinic activity and a significant difference in conformation as compared with acetylcholine. In the crystal structure the anions are oriented stereospecifically with respect to the tetrahedron of the quaternary ammonium group. The geometry of two triangles formed by the quaternary nitrogen atom, the oxygen atom of the carbonyl group, and by either of the two anions nearest to the quaternary ammonium group is characteristic for the nicotinic activity of 1.

Acetylcholine↗