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At least 19 recordsLinked to original sources
PubMed2000

State influences on ventral medullary surface and physiological responses to sodium cyanide challenges.

Intravenous sodium cyanide (NaCN) administration lowers ventral medullary surface (VMS) activity in anesthetized cats. Sleep states modify spontaneous and blood pressure-evoked VMS activity and may alter VMS responses to chemoreceptor input. We studied VMS activation during peripheral chemoreceptor stimulation by intravenous NaCN using optical procedures in six cats instrumented for recording sleep physiology during sham saline and control site trials. Images of scattered 660-nm light were collected at 50 frames/s with an optical device after 80-100 microg total bolus intravenous NaCN delivery during waking and sleep states. Cyanide elicited an initial ventilatory decline, followed by large inspiratory efforts and an increase in respiratory rate, except in rapid eye movement sleep, in which an initial breathing increase occurred. NaCN evoked a pronounced decrease in VMS activity in all states; control sites and sham injections showed little effect. The activity decline was faster in rapid eye movement sleep, and the activity nadir occurred later in waking. Sleep states alter the time course but not the extent of decline in VMS activity.

Animals↗
PubMedDate not supplied

Mechanism of action of sodium cyanide on rat diaphragm muscle.

The effects of sodium cyanide (NaCN) were investigated on the contractile and electrophysiological properties of rat diaphragm muscles in vitro. Sodium cyanide (0.1-1.0 mM) produced an initial potentiation of directly elicited twitch tensions, followed by a slow progressive depression. The potentiation and depression were both dependent on the NaCN concentration and stimulation frequency. Muscles exposed to NaCN exhibited marked reductions of creatine phosphate concentration, but ATP levels were not significantly lowered. Sodium cyanide had no effect on the resting potential, input resistance or action potential, indicating that the toxicity of the metabolic inhibitor is not mediated by alterations of membrane excitability or passive electrical properties. Sodium cyanide reduced the amplitude of contractures elicited by 70 mM K(2)SO(4), suggesting that the actions of NaCN cannot be explained by a failure of action potentials to propagate across the muscle surface or within t-tubular membranes. Sodium cyanide suppressed the first phase of the caffeine contracture, an observation consistent with an impaired release of, or reduced sensitivity to, sarcoplasmic reticular Ca(2+), but did not alter the amplitude of the second phase, which represents rigor following ATP depletion. These results, in conjunction with those of previous studies, suggest that the depression in muscle tension following exposure to NaCN may result from alterations in Ca(2+) homeostasis, intracellular acidosis or from accumulation of one or more products of phosphocreatine breakdown.

Acidosis↗
PubMed1991

On the inhibition of glutamic acid decarboxylase and gamma-aminobutyric acid transaminase by sodium cyanide.

The effects of sodium cyanide (NaCN) on the gamma-aminobutyric acid metabolizing enzymes glutamic acid decarboxylase (GAD) and gamma-aminobutyric acid transaminase (GABA-T) were studied in vitro. With no pyridoxal-5-phosphate added, GAD was non-competitively inhibited by NaCN, with an IC50 of 280 microM. GAD was also inhibited when exposed to an equimolar amount of NaCN and pyridoxal-5-phosphate. NaCN inhibited GABA-T. The inhibition kinetics suggests that NaCN may react with more than one of the substrates and products present during the reaction, i.e. pyridoxal-5-phosphate, alpha-ketoglutarate and/or succinic semialdehyde. The presence of pyridoxal-5-phosphate in the reaction mixture completely protected GABA-T from inhibition by NaCN. The gamma-aminobutyric acid synthesizing enzyme, GAD may thus be inhibited in vivo by NaCN or by a reaction product of NaCN and pyridoxal-5-phosphate. The gamma-aminobutyric acid catabolizing enzyme, GABA-T is not as vulnerable to inhibition by NaCN, since the cyanide-pyridoxal-5-phosphate complex is ineffective as inhibitor.

4-Aminobutyrate Transaminase↗
PubMed1993

NTP Toxicity Studies of Sodium Cyanide (CAS No. 143-33-9) Administered by Dosed Water to F344/N Rats and B6C3F1 Mice.

Cyanide and its salts are used extensively in industry and manufacturing and are found in water and food consumed by humans. Chronic exposure to low levels of cyanide is suspected to be responsible for various neuropathic and thyrotoxic conditions in humans. Data in the literature indicate that long-term exposure to near-lethal concentrations of cyanide may produce lesions in rodents similar to those linked to chronic cyanide exposure in humans. However, few data are available on the effects of subchronic exposure to cyanide concentrations that are not acutely toxic. To address this lack of data, 13-week toxicity studies on cyanide were conducted with male and female F344/N rats and B6C3F1 mice administered low doses of sodium cyanide in drinking water. Animals were evaluated for histopathology, clinical chemistry, hematology, urine chemistry, and reproductive toxicity. In addition, the mutagenicity of sodium cyanide was assessed in Salmonella typhimurium. Groups of 10 rats and 10 mice per sex were administered sodium cyanide in drinking water at concentrations of 0, 3, 10, 30, 100, and 300 ppm for 13 weeks. No deaths attributed to sodium cyanide administration occurred in either species. In animals exposed to 300 ppm, male rats had slightly lower final mean body weights and mean body weight gains and female mice had slightly lower final mean body weights than the respective controls. Water consumption by rats and mice in the 100 and 300 ppm groups was 10% to 30% lower than that by the controls; however, no clinical signs attributable to sodium cyanide administration or to dehydration were observed. No gross or microscopic changes specifically related to cyanide toxicity occurred at any site in males or females of either species. In particular, no lesions were found in the brain or thyroid gland. Differences between absolute and relative organ weights of exposed and control animals were minor and sporadic and were not exposure concentration dependent; these differences were not considered to be related to sodium cyanide administration. Hematologic, clinical chemistry, and urinalysis evaluations of rats and mice revealed minimal changes that were not considered biologically significant, although the decreased urine volume and increased urine specific gravity observed in male rats in the 300 ppm group of the supplemental clinical pathology study were consistent with the observed decreases in water consumption. The concentration of urinary thiocyanate (the primary metabolite of cyanide) increased with increasing exposure concentration at all time points. Sperm motility and vaginal cytology examinations were performed on rats and mice in the 0, 30, 100, and 300 ppm groups. Sodium cyanide caused a slight reduction in cauda epididymal weight in all groups of exposed male rats and in male mice exposed to 300 ppm. In male rats, the number of spermatid heads per testis in the 300 ppm group was less than the number in the controls, and sperm motility in all exposed groups was marginally lower than in the controls. Sodium cyanide produced no adverse effects on estrous cyclicity in female mice, but at higher concentrations (100 and 300 ppm), sodium cyanide caused a significant increase in the amount of time spent by female rats in proestrus and diestrus relative to estrus and metestrus. Sodium cyanide was not mutagenic in Salmonella typhimurium strain TA100, TA1535, TA97, or TA98 with or without exogenous metabolic activation. In summary, administration of low concentrations of sodium cyanide in drinking water to rats and mice for 13 weeks resulted in no clinically significant body weight, organ weight, histopathologic, or clinical pathology changes. The absorption of administered cyanide was confirmed by increases in urinary thiocyanate excretion. Concentrations of 100 ppm and greater resulted in reduced water consumption. Thus, higher concentrations of sodium cyanide could not be administered by the drinking water route of administration. Alterations in reproductive parameters indicate that subchronic exposure to low concentrations of sodium cyanide may produce mild but significant adverse effects on rat reproductive systems. These changes are probably insufficient to decrease fertility in rats; however, humans are considered to be relatively more sensitive to such changes than rats, and the potential for reproductive toxicity in humans from low concentrations of cyanide warrants further investigation. NOTE: These studies were supported in part by funds from the Comprehensive Environmental Response, Compensation, and Liability Act trust fund (Superfund) by an interagency agreement with the Agency for Toxic Substances and Disease Registry, U.S. Public Health Service.

Journal Article↗
PubMed1978

Sodium cyanide antagonism of the vasodilator action of sodium nitroprusside in theisolated rabbit aortic strip.

Resistance to sodium nitroprusside (SNP) is uncommon, but its occurrence has led to massive overdoses of SNP and sometimes death. To examine the mechanism responsible for resistance, aortic smooth muscle strips were prepared and dose-response curves for norepinephrine (NE) obtained. SNP alone caused a shift of the dose-response curve for NE to the right. However, this shift was less when the strips were exposed to both SNP and sodium cyanide (CN-). When CN- alone was added to the aortic strips, the response to NE was unchanged. In a further group of aortic muscle strips first contracted with NE and then relaxed with SNP, the addition of CN- caused the muscles to contract again. It is concluded that CN- antagonizes the action of SNP in vitro, and that this antagonism is specific for SNP.

Animals↗
PubMed2003

Pulsatilloside A and anemoside A3 protect PC12 cells from apoptosis induced by sodium cyanide and glucose deprivation.

Using sodium cyanide (NaCN) and glucose deprivation induced cell injury in PC12 as an injury model, we investigated the protective effects of pulsatilloside A and anemoside A 3 on neurons. The results showed that PC12 cells under the NaCN-injury and glucose deprivation would undergo apoptosis. Additions of pulsatilloside A and anemoside A 3, at dosages ranging from 0.1, 1 and 10 microg/ml, protected PC12 cells from apoptosis determined by MTT, LDH release analysis, and flow cytometry measurement.

Alzheimer Disease↗
PubMed2005

Rapid sodium cyanide depletion in cell culture media: outgassing of hydrogen cyanide at physiological pH.

During the course of in vitro studies on cyanide exposure with SH-SY5Y human neuroblastoma cells, we found that sodium cyanide (NaCN) up to a concentration of 10 mM had no significant toxic effect under our culture conditions. Further investigation of this apparent cyanide resistance revealed that the sodium cyanide was being rapidly depleted from the cell culture medium. Cyanide was interacting with constituents of the cell culture medium and was somehow being detoxified or removed from solution. The reaction of cyanide with cell culture media in 96-well culture plates reduced cyanide concentrations rapidly (80-90% in 2 h at 37 degrees C). Running the same reaction in capped tubes significantly reduced cyanide loss from solution. Incubation of cyanide with individual constituents of the cell culture medium in solution showed that glucose, phenol red, and amino acids all acted to detoxify or remove cyanide from solution. When amino acids or buffers were incubated with sodium cyanide in aqueous solution at pH 7.4, hydrogen cyanide (HCN) was found to degas from the solutions. We compared HCN outgassing over a range of pH values. As expected, HCN remained very soluble at high pH, but as the pH was reduced to 7.0, the rate of HCN formation and outgassing increased dramatically. Acid-base reactions involving cyanide and proton donors, such as amino acids and other cell culture media constituents, at physiological pH result in rapid HCN outgassing from solution at 37 degrees C. These results indicate that previous in vitro cyanide toxicity studies done in standard culture media with prolonged incubation times using gas-exchanging culture containers might have to be reevaluated in light of the fact that the effective cyanide concentrations in the culture media were significantly lower than reported.

Culture Media↗
PubMed2004

[Two suicide fatalities from sodium cyanide ingestion: differences in blood biochemistry].

We report a case of two suicide fatalities from sodium cyanide ingestion, which showed differences in pathology and blood biochemistry. The victims were a married couple in their 70 years of age, owners of a gilding factory. They were found dead in their bedroom by a family member. Suicide notes and sodium cyanide powder were found in the room. Autopsy revealed eroded gastric mucosae in both victims. In the male, the stomach showed a previous postoperative state of partial resection, and the lungs were more congested and edematous in the male than in the female. In both victims, cyanide was detected in the blood at markedly high concentrations. In postmortem blood biochemistry, a marked elevation of cardiac troponin T, I and CK-MB was observed in the peripheral blood of the male, whereas there was only a mild elevation in the female. In the male, erythropoietin was also markedly elevated. These observations suggested a difference in the dying process following sodium cyanide ingestion between the victims; survival time may have been longer in the male than the female. The absorption of cyanide may have been a contributory factor to the difference.

Aged↗
PubMedDate not supplied

[The effect of sodium cyanide and its antidotes on the isolated perfused rat heart].

The experiments were performed to investigate the effects of cyanide and several antidotes (sodium nitrite, DMAP, sodium thiosulfate and phentolamine) on isolated perfused rat heart to further elucidate the mechanism of action of cyanide and its antidotes. Sodium cyanide (40, 50 and 60 mg/ml) produced maximum effects on amplitude, heart rate and coronary flow, after 3 min, regardless of the event recorded. Some dose-dependence was noted, especially on the heart rate, somewhat less on amplitude and almost none on the coronary flow up to 15 min, but notable afterwards. Some spontaneous recovery occurred in each event, the most significant being that of the heart rate. Antidotes per se did not differ significantly in their action on isolated rat heart. All values, with some variations, were maintained within 10-20% of control. Antidotes, injected 1 min after sodium cyanide produced the most evident effects on amplitude and heart rate -- all antidotes practically and almost instantly neutralized the depressant effect of cyanide. Nitrite and particularly DMAP, were the most effective on coronary flow while other antidotes, although effective up to 3 min, did not much differ from cyanide alone throughout the rest of observation.

Aminophenols↗
PubMed2005

Mechanistic studies on the decomposition of sodium cyanide in aqueous solution and in the solid state.

The mechanism of the spontaneous decomposition of sodium cyanide in aqueous solution and in the solid state was studied by ion chromatography (IC), FT-Raman spectroscopy, gas chromatography/mass spectrometry (GC/MS), and carbon-13 nuclear magnetic resonance spectroscopy (13C NMR). In the aqueous solution, gradual decomposition of the cyanide to carbonate by a displacement reaction was observed. In the solid state, sodium cyanide was found to be stable when kept in dry air, however, it decomposed by the same mechanism as that in aqueous solution under non-dry conditions.

Journal Article↗
PubMed2003

Aerobic ruthenium-catalyzed oxidative cyanation of tertiary amines with sodium cyanide.

RuCl3-catalyzed oxidative cyanation of tertiary amines with sodium cyanide under molecular oxygen (1 atm) at 60 degrees C gives the corresponding alpha-aminonitriles, which are versatile synthetic intermediates of various compounds such as amino acids and unsymmetrical 1,2-diamines, in excellent yields. This reaction is clean and should be an environmentally benign and useful process.

Amines↗
PubMed1992

Cardiorespiratory changes induced by vertebral artery injection of sodium cyanide in cats.

Brain stem hypoxia caused by vertebral artery injection of sodium cyanide (NaCN) (1-20 micrograms) in artificially ventilated cats depressed phrenic and stimulated sympathetic nerve activity with a simultaneous increase in arterial blood pressure. Larger doses of NaCN caused greater effects. Hypercapnia produced by inhalation of 7% CO2 in O2 tended to reduce NaCN-induced responses on phrenic activity but not on blood pressure or sympathetic activity. Infusion into the vertebral artery with hypoxic saline (3% CO2 in N2) altered blood pressure, also affecting phrenic and sympathetic nerves similarly to NaCN administration. However, washout of CO2 by infusion of 100% O2 bubbled saline at high flow rates (3.6 ml/min) depressed phrenic as well as sympathetic activity and blood pressure. Spinal transection at the first cervical level eliminated sympathetic excitatory response to intravertebral cyanide injection. However, a large dose of NaCN (600 micrograms) given intravenously in spinal animal excited sympathetic activity. We conclude that intravertebral injection of NaCN can be used to study the effects of local hypoxia of the brain stem on cardiorespiratory responses and that hypoxia acts at both these sites (brain stem and spinal cord) to stimulate sympathetic excitation.

Animals↗