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PubMed1969

The effect of cyanide on the efflux of calcium from squid axons.

1. The average rate constant for loss of (45)Ca from an unpoisoned squid axon was 1.8 x 10(-3) min(-1), corresponding to an efflux of 0.2 p-mole/cm(2) sec.2. The Ca efflux from unpoisoned axons was reduced if external calcium was replaced with magnesium, or external sodium with lithium, choline or dextrose. Replacing both sodium and calcium reduced the efflux to about 40%.3. Cyanide caused little immediate change in Ca efflux but after 1(1/2)-2(1/2) hr the efflux increased to 5-15 times its normal value. The effect was rapidly reversed when cyanide was removed.4. The large Ca efflux into cyanide was reduced by a factor of three when external calcium was replaced with magnesium and by a further factor of about six when external sodium was replaced with lithium.5. The Ca efflux from both poisoned and unpoisoned axons had a Q(10) of 2-3, was not affected by ouabain and was greatly reduced by injecting ethyleneglycol bis (aminoethylether)-N,N'-tetra-acetic acid (EGTA).6. After injecting (45)Ca along the axis, the efflux of calcium reached its maximum much more rapidly in a cyanide-treated axon than in an unpoisoned axon.7. Pre-treatment with cyanide greatly increased the rate at which calcium was lost from axoplasm extruded into flattened dialysis bags. A similar effect was observed when cyanide was applied after extrusion.8. Replacing external sodium glutamate with potassium glutamate greatly reduced the loss of (45)Ca from intact axons poisoned with cyanide but had little effect on the loss from extruded axoplasm.9. The rate constant for loss of the Ca EGTA complex was about 3 x 10(-5) min(-1) for intact axons and 2 x 10(-2) min(-1) for extruded axoplasm.10. A possible explanation of the cyanide effect is that, after poisoning, calcium ions are released from a store and can then exchange at a higher rate with external sodium or calcium.11. The experiments suggest that part of the calcium efflux may be coupled to sodium entry.12. Theoretical equations for ;diffusion and chemical reaction in a cylinder' are described in the Appendix.

Animals↗
PubMed2006

Involvement of Pseudomonas aeruginosa rhodanese in protection from cyanide toxicity.

Cyanide is a serious environmental pollutant and a biocontrol metabolite in plant growth-promoting Pseudomonas species. Here we report on the presence of multiple sulfurtransferases in the cyanogenic bacterium Pseudomonas aeruginosa PAO1 and investigate in detail RhdA, a thiosulfate:cyanide sulfurtransferase (rhodanese) which converts cyanide to less toxic thiocyanate. RhdA is a cytoplasmic enzyme acting as the principal rhodanese in P. aeruginosa. The rhdA gene forms a transcriptional unit with the PA4955 and psd genes and is controlled by two promoters located upstream of PA4955 and rhdA. Both promoters direct constitutive RhdA expression and show similar patterns of activity, involving moderate down-regulation at the stationary phase or in the presence of exogenous cyanide. We previously observed that RhdA overproduction protects Escherichia coli against cyanide toxicity, and here we show that physiological RhdA levels contribute to P. aeruginosa survival under cyanogenic conditions. The growth of a DeltarhdA mutant is impaired under cyanogenic conditions and fully restored upon complementation with rhdA. Wild-type P. aeruginosa outcompetes the DeltarhdA mutant in cyanogenic coculture assays. Hence, RhdA could be regarded as an effector of P. aeruginosa intrinsic resistance to cyanide, insofar as it provides the bacterium with a defense mechanism against endogenous cyanide toxicity, in addition to cyanide-resistant respiration.

Amino Acid Sequence↗
PubMed1991

Novel cyanide-hydrolyzing enzyme from Alcaligenes xylosoxidans subsp. denitrificans.

A cyanide-metabolizing bacterium, strain DF3, isolated from soil was identified as Alcaligenes xylosoxidans subsp. denitrificans. Whole cells and cell extracts of strain DF3 catalyzed hydrolysis of cyanide to formate and ammonia (HCN + 2H2O----HCOOH + NH3) without forming formamide as a free intermediate. The cyanide-hydrolyzing activity was inducibly produced in cells during growth in cyanide-containing media. Cyanate (OCN-) and a wide range of aliphatic and aromatic nitriles were not hydrolyzed by intact cells of A. xylosoxidans subsp. denitrificans DF3. Strain DF3 hydrolyzed cyanide with great efficacy. Thus, by using resting induced cells at a concentration of 11.3 mg (dry weight) per ml, the cyanide concentration could be reduced from 0.97 M (approximately 25,220 ppm) to less than 77 nM (approximately 0.002 ppm) in 55 h. Enzyme purification established that cyanide hydrolysis by A. xylosoxidans subsp. denitrificans DF3 was due to a single intracellular enzyme. The soluble enzyme was purified approximately 160-fold, and the first 25 NH2-terminal amino acids were determined by automated Edman degradation. The molecular mass of the active enzyme (purity, greater than 97% as determined by amino acid sequencing) was estimated to be greater than 300,000 Da. The cyanide-hydrolyzing enzyme of A. xylosoxidans subsp. denitrificans DF3 was tentatively named cyanidase to distinguish it from known nitrilases (EC 3.5.5.1) which act on organic nitriles.

Alcaligenes↗
PubMed1993

Isolation and characterization of a cyanide dihydratase from Bacillus pumilus C1.

A cyanide-degrading enzyme from Bacillus pumilus C1 has been purified and characterized. This enzyme consisted of three polypeptides of 45.6, 44.6, and 41.2 kDa; the molecular mass by gel filtration was 417 kDa. Electron microscopy revealed a multimeric, rod-shaped protein approximately 9 by 50 nm. Cyanide was rapidly degraded to formate and ammonia. Enzyme activity was optimal at 37 degrees C and pH 7.8 to 8.0. Activity was enhanced by Sc3+, Cr3+, Fe3+, and Tb3+; enhancement was independent of metal ion concentration at concentrations above 5 microM. Reversible enhancement of enzymatic activity by azide was maximal at 4.5 mM azide and increased with time. No activity was recorded with the cyanide substrate analogs CNO-, SCN-, CH3CN, and N3- and the possible degradation intermediate HCONH2. Kinetic studies indicated a Km of 2.56 +/- 0.48 mM for cyanide and a Vmax of 88.03 +/- 4.67 mmol of cyanide per min/mg/liter. The Km increased approximately twofold in the presence of 10 microM Cr3+ to 5.28 +/- 0.38 mM for cyanide, and the Vmax increased to 197.11 +/- 8.51 mmol of cyanide per min/mg/liter. We propose naming this enzyme cyanide dihydratase.

Bacillus↗
PubMed1995

Isolation and characterization of mutants defective in the cyanide-insensitive respiratory pathway of Pseudomonas aeruginosa.

The branched respiratory chain of Pseudomonas aeruginosa contains at least two terminal oxidases which are active under normal physiological conditions. One of these, cytochrome co, is a cytochrome c oxidase which is completely inhibited by concentrations of the respiratory inhibitor potassium cyanide as low as 100 microM. The second oxidase, the cyanide-insensitive oxidase, is resistant to cyanide concentrations in excess of 1 mM as well as to sodium azide. In this work, we describe the isolation and characterization of a mutant of P. aeruginosa defective in cyanide-insensitive respiration. This insertion mutant was isolated with mini-D171 (a replication-defective derivative of the P. aeruginosa phage D3112) as a mutagen and by screening the resulting tetracycline-resistant transductants for the loss of ability to grow in the presence of 1 mM sodium azide. Polarographic studies on the NADH-mediated respiration rate of the mutant indicated an approximate 50% loss of activity, and titration of this activity against increasing cyanide concentrations gave a monophasic curve clearly showing the complete loss of cyanide-insensitive respiration. The mutated gene for a mutant affected in the cyanide-insensitive, oxidase-terminated respiratory pathway has been designated cio. We have complemented the azide-sensitive phenotype of this mutant with a wild-type copy of the gene by in vivo cloning with another mini-D element, mini-D386, carried on plasmid pADD386. The complemented cio mutant regained the ability to grow on medium containing 1 mM azide, titration of its NADH oxidase activity with cyanide gave a biphasic curve similar to that of the wild-type organism, and the respiration rate returned to normal levels. Spectral analysis of the cytochrome contents of the membranes of the wild type, the cio mutant, and the complemented mutant suggests that the cio mutant is not defective in any membrane-bound cytochromes and that the complementing gene does not encode a heme protein.

Azides↗
PubMed1975

Nonperipheral chemoreceptor stimulation of ventilation by cyanide.

To assess the ventilatory responses elicited by changes of tissue hypoxia, sodium cyanide (0.12 mg/kg-min for 10 min) was infused into the upper abdominal aorta of anesthetized dogs. These infusions produced decreases in oxygen consumption, increases in arterial lactate concentration, and increases in arterial lactate/pyruvate ratio. Coincident with these metabolic changes of hypoxia, minute ventilation (VE) increased 228 +/- SE 36% and arterial PCO2 decreased 21 +/- SE 2 mmHg; therefore, pH increased both in arterial blood in and cisternal cerebrospinal fluid. Following infusion of cyanide into the abdominal aorta, small quantities of cyanide (48 +/- SE 14 mumol/liter) appeared in carotid arterial blood. To evaluate the possibility that the observed increases in VE were due to stimulation of peripheral arterial chemoreceptors by the recirculating cyanide, the carotid and aortic chemoreceptors were denervated in four dogs. Nonetheless, after intra-aortic infusion of sodium cyanide (1.2 mg/kg), ventilation in these chemodenervated animals again increased considerably (154 +/- SE 36%). In order to explore the possibility that cyanide infusion can stimulate ventilation by an extracranial mechanism, heads of vagotomized dogs (including the carotid bodies) were perfused entirely by donor dogs. The intra-aortic infusion of sodium cyanide (0.9 mg/kg) into these head-perfused animals still caused large increases in VE (163 +/- SE 19%). It is concluded that intra-aortic cyanide infusions stimulate VE by an extracranial mechanism other than the carotid and aortic chemoreceptors.

Animals↗
PubMed1999

Mercaptopyruvate sulfurtransferase as a defense against cyanide toxication: molecular properties and mode of detoxification.

In cyanide poisoning, metalloproteins and carbonyl groups containing proteins are the main target molecules of nucleophilic attack by cyanide. To defend against this attack, cyanide is metabolized to less toxic thiocyanate via transsulfuration. This reaction is catalyzed by rhodanese and mercaptopyruvate sulfurtransferase (MST). Rhodanese is a well characterized mitochondrial enzyme. On the other hand, little was known about MST because it was unstable and difficult to purify. We first purified MST to homogeneity and cloned MST cDNA from rat liver to characterize MST. We also found that MST was an evolutionarily related enzyme of rhodanese. MST and rhodanese are widely distributed in rat tissues, and the kidney and liver prominently contain these enzymes. Immunohistochemical study revealed that MST is mainly distributed in proximal tubular epithelial cells in the kidney, pericentral hepatocytes in the liver, the perinuclear area of myocardial cells in the heart, and glial cells in the brain, and immunoelectron microscopical study concluded that MST was distributed in both cytoplasm and mitochondria, so that MST first detoxifies cyanide in cytoplasm and the cyanide which escapes from catalysis due to MST enters mitochondria. MST then detoxifies cyanide again in cooperation with rhodanese in mitochondria. Tissues other than the liver and kidney are more susceptible to cyanide toxicity because they contain less MST and rhodanese. Even in the same tissue, sensitivity to cyanide toxicity may differ according to the kind of cell. It is determined by a balance between the amount of proteins to be attacked and that of enzymes to defend.

Amino Acid Sequence↗
PubMed2006

Pediatric cyanide poisoning: causes, manifestations, management, and unmet needs.

Confirmed cases of childhood exposure to cyanide are rare despite multiple potential sources including inhalation of fire smoke, ingestion of toxic household and workplace substances, and ingestion of cyanogenic foods. Because of its infrequent occurrence, medical professionals may have difficulty recognizing cyanide poisoning, confirming its presence, and treating it in pediatric patients. The sources and manifestations of acute cyanide poisoning seem to be qualitatively similar between children and adults, but children may be more vulnerable than adults to poisoning from some sources. The only currently available antidote in the United States (the cyanide antidote kit) has been used successfully in children but has particular risks associated with its use in pediatric patients. Because hemoglobin kinetics vary with age, methemoglobinemia associated with nitrite-based antidotes may be excessive at standard adult dosing in children. A cyanide antidote with a better risk/benefit ratio than the current agent available in the United States is desirable. The vitamin B12 precursor hydroxocobalamin, which has been used in Europe, may prove to be an attractive alternative to the cyanide antidote kit for pediatric patients. In this article we review the available data on the sources, manifestations, and treatment of acute cyanide poisoning in children and discuss unmet needs in the management of pediatric cyanide poisoning.

Adolescent↗
PubMed2006

Modelling anaerobic digestion acclimatisation to a biodegradable toxicant: application to cyanide.

The observed acclimatisation to biodegradable toxicants in anaerobic cassava wastewater treatment is explained by modelling anaerobic cyanide degradation. A complete degradation pathway is proposed for cyanide. Cyanide degradation is modelled as enzymatic hydrolysis to formate and ammonia. Ammonia is added to the inorganic nitrogen content of the digester while formate is degraded by the hydrogenotrophic methanogens. Cyanide irreversible enzyme inhibition is modelled as an inhibition factor to acetate uptake processes. Cyanide irreversible toxicity is modelled as a decay factor to the acetate degraders. Cyanide as well as added phosphorus buffer solution were considered in the chemical equilibrium calculations of pH. The observed reversible effect after acclimatisation of sludge is modelled by a population shift between two aceticlastic methanogens that have different tolerance to cyanide toxicity. The proposed pathway is added to the IWA Anaerobic Digestion Model no.1 (ADM1). The ADM1 model with the designed extension is validated by an experiment using three lab-scale upflow anaerobic sludge bed reactors which were exposed to different cyanide loadings.

Anaerobiosis↗
PubMedDate not supplied

Formation of free cyanide and cyanogen chloride from chloramination of publicly owned treatment works secondary effluent: laboratory study with model compounds.

The potential generation of cyanide species in wastewater upon chlorination in the presence of residual ammonia (resulting in chloramine formation) was investigated in experiments with synthetic solutions and publicly owned treatment works (POTW) secondary effluent. This study demonstrated that low concentrations (approximately 5 to 25 microg/L as cyanide) of cyanogen chloride (CNCI), a highly toxic cyanide species not measured in total or free cyanide analyses, could be detected as a result of chloramination reactions in POTW secondary effluent. The potential for chloramination of nitrogen-bearing organic compounds to yield CNCl and/or free cyanide was demonstrated in experiments with synthetic solutions spiked with selected precursor organics: L-serine, benzene, catechin, and humic acid. The amino acid L-serine yielded the largest concentrations of CNCI upon chloramination. Additionally, detectable cyanide (approximately 10 microg/L) was observed in solutions of L-serine and in POTW secondary effluent that was chloraminated followed by dechlorination to prevent destruction of any free cyanide produced. Thus, chlorination of POTW secondary effluent containing residual ammonia can lead to chloramination of organic compounds and the resulting production of CNCl and free cyanide.

Ammonia↗
PubMedDate not supplied

Effects of nitrosation on the formation of cyanide in publicly owned treatment works secondary effluent.

Cyanide has been detected in the effluents of some publicly owned treatment works (POTWs) at levels exceeding the influent concentration. The presence of nitrite ion (NO2-) as a common constituent in domestic wastewater effluents may play an important role in the formation of cyanide through reaction with certain kinds of organic compounds, especially aromatic compounds. Laboratory studies with seven organic compounds (aniline. p-toluidine, phenol, 1,2,4-trihydroxybenzene, L-serine, glycine, and benzoic acid) revealed that cyanide can be formed by reaction of nitrite with some of these compounds. The most substantial free cyanide (HCN. CN-) production observed at 25 degrees C was 0.15 mg/L from reaction of 0.01 mM 1.2.4-trihydroxybenze with 5 mg/L nitrite for 72 hours. Substantial free cyanide formation was also observed at pH 2-4 in experiments with POTW effluents when reactive organics and nitrite were both added to wastewater. Formation of cyanide through nitrosation was strongly pH dependent, being most significant at low pH (2 to 4) and negligible at neutral-to-high pH. This result points to nitrous acid (HNO2) as being more reactive than the dissociated NO2- ion. The reaction of these nitrite species with organics also occurs in conventional analyses for total cyanide which involve distillation under strongly acidic conditions. Sufficient sample pretreatment with sulfamic acid at the time of sampling, not at the time of analysis. is highly recommended to prevent biasing analytical measurement of total cyanide in POTW effluents.

Cyanides↗
PubMed2001

[The distribution and natural degradation of cyanide in goldmine waste-solid and polluted soil].

The farmland and river were seriously polluted by cyanide because one goldmine tailing dam collapsed in 1995. 3 and 4 years after the accident, the cyanide distribution in the polluted farmland and the abandoned tailing dam was studied. The results indicated that natural degradation of cyanide in soil section was slower than in natural water body. The cyanide transference in soil section was similar to freely soluble salts. In arid and semiarid area, cyanide can be highly enriched in the salt shell which content degrading 4 years even higher than the fresh tailing slurry. One side the viscidity layer in the soil section can partly prevent cyanide transference to groundwater, on the other side the result can cause the cyanide highly enrich in the viscidity layer. According to character of cyanide natural degradation in soil the measurement of prevention and cure soil pollution by goldmine tailing dam collapsing was brought forward.

Cyanides↗
PubMedDate not supplied

Methacrylonitrile: in vivo metabolism to cyanide in rats, mice, and gerbils.

Methacrylonitrile (MeAN), a widely used industrial chemical, is metabolized to cyanide in rats, mice, and gerbils. Cyanide levels following oral administration of 0.5 or 1 LD50 dose of MeAN were determined in blood and organs of treated animals. Male Mongolian gerbils were 50-fold more sensitive to MeAN than Sprague-Dawley rats and about 5-fold more sensitive than were Albino-Swiss mice. The signs of MeAN toxicity were typically those of cyanide-related central nervous system poisoning in all the three species. The difference was in the time required for the onset of these signs. Mice and gerbils developed the toxicity signs faster than the rats. All the three species showed a dose-response relationship in metabolism of MeAN to cyanide. However, in mice and gerbils, the peak blood concentration of cyanide occurred 1 hr following MeAN administration, whereas it took 3 hr for rats to reach peak blood cyanide levels. In the rats treated with phenobarbital or those starved for 18 hr, the metabolism of MeAN to cyanide increased significantly (159-178% and 181-201% of control, respectively), and the treatment of rats with CoCl2 resulted in a significant decrease in MeAN metabolism to cyanide (60-68% of control). These studies indicate a distinct species difference in the toxicity and metabolism of MeAN.

Animals↗
PubMed1991

Cyanide intoxication in mice through different routes and its prophylaxis by alpha-ketoglutarate.

Antagonising effects of alpha-ketoglutarate (alpha-KG) could be attributed to complexing of the reactive nucleophile (CN-) to form cyanohydrin in cyanide intoxication. However, an enormous protection obtained could not be delineated on account of possible in situ binding of alpha-KG given intraperitoneally (i.p.) in mice to cyanide administered through the same route. The present study was designed to see the efficacy of alpha-KG alone or in combination with sodium nitrite (SN) and/or sodium thiosulfate (STS) in male mice exposed to cyanide administered through subcutaneous (s.c.) or inhalation route. A technique for generation of hydrogen cyanide (HCN) is also discussed. On the basis of protection index (PI), defined here as the LD50 of cyanide in protected mice/LD50 of cyanide in unprotected mice and survival time, STS + alpha-KG regimen was equipotent to the conventional SN + STS regimen. This is further substantiated by effect of alpha-KG in reducing plasma cyanide levels. The efficacy of alpha-KG remains undeterred irrespective of the route of cyanide intoxication, while the magnitude of protection varies.

Animals↗
PubMed1991

Treatment of cyanide poisoning.

The object of this study was to evaluate the effectiveness of five regimens in treating cyanide poisoning. A series of anesthetized adult beagle dogs were instrumented to record hemodynamic and respiratory function and given 2.5 mg/kg sodium cyanide intravenously. The 10 control animals given only cyanide died at from 5 to 7 minutes. Therapy, as described below, was given to other groups at from 2 to 3 minutes following the cyanide administration. Artificial respiration did not alter the lethal effects of cyanide nor prolong survival time in any of the 10 animals. Amyl nitrite given by inhalation or by the intravenous route allowed survival of all 15 animals. Sodium nitrite (20 mg/kg), dimethylaminophenol (DMAP) (5 mg/kg), and hydroxylamine hydrochloride (5 mg/kg) given intravenously with no artificial ventilation also allowed for 100% survival (15 animals). Amyl nitrite, sodium nitrite, and sodium thiosulfate were ineffective when given intramuscularly (I.M.) (0 of 12 dogs); however, I.M. DMAP (5 mg/kg) and I.M. hydroxylamine hydrochloride (50 mg/kg) increased heart rate and blood pressure and restored spontaneous breathing. All 15 animals treated with I.M. doses of either of these drugs survived the lethal dose of cyanide. Results of these studies indicate that intravenous sodium nitrite, DMAP, and hydroxylamine hydrochloride, and amyl nitrite by inhalation, are all effective in reversing the lethal effects of cyanide poisoning. Only DMAP and hydroxylamine hydrochloride are effective when given by the intramuscular route. These results provide data to support an approach to therapy that is more practical and applicable where expert medical care may not be available following cyanide exposure.

Animals↗
PubMed1989

Cyanide poisoning: pathophysiology and current approaches to therapy.

Considering the difficulties following the administration of nitrites (or aminophenols) or cobalt-EDTA as well as the ineffectivenes of hydroxycobalamin and pyruvate, we feel that a more sensible treatment for acute cyanide intoxication is hemodialysis combined with the intravenous administration of sodium thiosulfate. The addition of hemodialysis to such a regimen is helpful in three ways. First, it removes the small extracellular reservoir of cyanide, particularly if the poison is still being absorbed from the gastrointestinal tract. Second, it corrects the severe lactic acidosis seen in virtually all cases of cyanide toxicity. As with most poisons death from metabolic acidosis alone is likely. Third, the removal of thiocyanate, the end product of cyanide metabolism, results in a maneuver which should decrease both tissue and plasma cyanide levels. The immediate treatment of acute cyanide intoxication is supportive, as it is with most all drugs and poisons. Gastric lavage using activated charcoal should be initiated immediately to remove any remaining cyanide in the gastrointestinal tract. Simultaneously, high flow oxygen should be administered either by nasal cannula or by endotracheal intubation. Correction of the metabolic acidosis should be instituted with bicarbonate. Immediate hemodialysis should be performed with the concomitant administration of thiosulfate. Animal studies suggest that continuous infusion of thiosulfate (12 mg/kg/hr) is more effective for treating cyanide intoxication than is bolus administration (41, 51). Bolus administration is the currently recommended form of thiosulfate therapy in humans. The Lilly kit contains a 50 ml ampule of thiosulfate having 12.5 gm, which in adults may be repeated once at one-half the dose.(ABSTRACT TRUNCATED AT 250 WORDS)

Cyanides↗
PubMed1986

Dissimilarities between methylene blue and cyanide on relaxation and cyclic GMP formation in endothelium-intact intrapulmonary artery caused by nitrogen oxide-containing vasodilators and acetylcholine.

The objective of the present study was to ascertain whether cyanide shares the properties of methylene blue as a selective inhibitor of vascular smooth muscle relaxation elicited by agents that stimulate the formation of cyclic GMP. Experiments were performed with endothelium-intact rings prepared from bovine intrapulmonary artery. Methylene blue, a good inhibitor of soluble guanylate cyclase, antagonized both arterial relaxation and cyclic GMP accumulation in response to sodium nitroprusside, glyceryl trinitrate, S-nitroso-N-acetylpenicillamine and acetylcholine. In contrast, cyanide inhibited only the responses to sodium nitroprusside. Increasing concentrations of methylene blue depressed resting arterial levels of cyclic GMP and caused slowly developing but marked contractions whereas cyanide was without effect. Contractile responses to phenylephrine, potassium and U46619 were potentiated by methylene blue but not by cyanide. Preincubation of dilute solutions of cyanide containing sodium nitroprusside in oxygenated Krebs' buffer at 37 degrees C for 15 min before addition to bath chambers depressed relaxation and cyclic GMP accumulation caused by sodium nitroprusside markedly. Similar treatment of glyceryl trinitrate, however, failed to alter its effects in arterial rings. A chemical inactivation of sodium nitroprusside by cyanide appears to account for the specific inhibitory action of cyanide on arterial responses to sodium nitroprusside. This study indicates clearly that cyanide does not share the properties of methylene blue as an inhibitor of arterial relaxation elicited by vasodilators that stimulate cyclic GMP formation.

Acetylcholine↗
PubMed1988

In vitro cyanide release from sodium nitroprusside in various intravenous solutions.

The concentration of cyanide, a toxic metabolite of sodium nitroprusside, in solutions other than 5% dextrose in water, has not been reported. In this study, cyanide ion levels were measured by a cyanide ion-specific electrode in 250 ml of six different intravenous solutions (5% dextrose in water, 10% dextrose in water, distilled water, 0.9% sodium chloride, and lactated Ringer's solution with and without 5% dextrose) exposed to 300 foot candles of fluorescent light for 72 hours after sodium nitroprusside was dissolved in each solution. The rates of the increase in cyanide ion concentration in all six solutions were fairly constant between 4 and 24 hours. At 24 hours, there were no statistically significant differences in cyanide ion concentration among the six solutions. After 24 hours, the rate of the increase in cyanide ion concentration in the electrolyte solutions decreased more than that in the nonelectrolyte solutions. At 72 hours, the electrolyte-containing solutions had statistically significant lower mean cyanide ion concentrations than 5% dextrose, often the recommended diluent for sodium nitroprusside. There was no difference in mean cyanide ion concentration between lactated Ringer's solution with and without 5% dextrose. Solutions containing electrolytes are preferable to 5% dextrose for the dilution of sodium nitroprusside.

Cyanides↗