Sodium Cyanide

A highly poisonous compound that is an inhibitor of many metabolic processes and is used as a test reagent for the function of chemoreceptors. It is also used in many industrial processes.

Also Known As:

Networked: 106 relevant articles (2 outcomes, 8 trials/studies)

Relationship Network

Bio-Agent Context: Research Results

Experts

1.	Solomon, Irene C: 3 articles (05/2005 - 03/2002)
2.	Milsom, William K: 2 articles (01/2015 - 04/2005)
3.	Gilmour, Kathleen M: 2 articles (01/2010 - 04/2005)
4.	Perry, Steve F: 2 articles (01/2010 - 04/2005)
5.	Li, Yansong: 2 articles (01/2010 - 03/2008)
6.	Tsokos, George C: 2 articles (01/2010 - 12/2003)
7.	Yamazaki, T: 2 articles (05/2008 - 05/2000)
8.	Akiyama, T: 2 articles (05/2008 - 05/2000)
9.	Kiang, Juliann G: 2 articles (03/2008 - 12/2003)
10.	Brink, Deidre L: 1 article (01/2015)

Related Diseases

1.	Anoxia (Hypoxia) 03/17/2011 - "Therefore, in the present study, we investigated the activity of glutamatergic and GABAergic mechanisms from the CPA and commNTS in rats exposed to hypoxia and the effects of the inhibition of CPA neurons on cardiorespiratory responses to peripheral chemoreceptor activation with i.v. sodium cyanide (NaCN). " 01/01/2010 - "The present study investigates the ability of DAF to protect primary cultured neuronal cells subjected to sodium cyanide (NaCN)-induced hypoxia from degeneration and apoptosis. " 07/01/1997 - "We conclude from our experiments that sodium cyanide is useful to study hypoxic injury and that cerebral endothelial cells are more sensitive than non-cerebral endothelial cells to cytotoxic hypoxia." 01/01/2014 - "Following a pre-treatment with low dosage sodium cyanide (10-20μM), the hypoxia-induced nerve response was significantly reduced along with hypoxia-induced catecholamine release. " 03/01/2008 - "To determine whether iNOS and NO production are responsible for chemical hypoxia-induced apoptosis, we exposed human Jurkat T cells to sodium cyanide in the presence or absence of iNOS inhibitors. "
2.	Hypercapnia 09/01/2000 - "CDN lesions did not significantly alter eupneic breathing, but FN lesions attenuated the respiratory response to hypercapnia and sodium cyanide. " 05/01/1981 - "Moreover, in contrast to eupnea or apneusis, neither the frequency nor the intensity of gasps was altered by hypercapnia, hypocapnia, or carotid chemoreceptor stimulation by sodium cyanide. " 10/01/1981 - "These stimuli were intracarotid infusions of sodium cyanide or nicotine and exposure to hyperoxic hypercapnia, respectively. " 10/01/1993 - "The responses to acidic hypercapnia (PCO2 = 50-60 Torr, pH = 7.20-7.10), hypoxia (PO2 = 25 and 50 Torr), perfusate flow interruption, and bolus injections of sodium cyanide (20-40 nmol) were tested. " 04/15/2005 - "Tambaqui were exposed to periods of normoxia, hypoxia, hyperoxia and hypercapnia during which, externally oriented O2 and CO2 chemoreceptors were further stimulated, by administration into the inspired water of sodium cyanide and CO2-equilibrated water, respectively. "
3.	Poisoning 01/01/2011 - "The authors report here the case of a man who was the victim of occupational poisoning with sodium cyanide and who was treated at the workplace by fire-fighters and the Service Mobile d'Urgence et Reanimation emergency ambulance service." 10/01/1986 - "Sensitivities of six avian species, black vulture (Coragyps atratus), American kestrel (Falco sparverius), Japanese quail (Coturnix japonica), domestic chicken (Gallus domesticus), eastern screech-owl (Otus asio), and European starling (Sturnus vulgaris), to acute poisoning by sodium cyanide (NaCN) were compared by single dose LD50's. " 11/01/1970 - "[Skin lesions in a case of acute fatal sodium cyanide poisoning]." 02/25/1969 - "[Successful treatment of acute accidental sodium cyanide poisoning]." 01/01/1954 - "[Lesions associated with hardening of steel; report of acute case of poisoning with sodium cyanide]."
4.	Ischemia 01/01/1994 - "Fifteen hearts underwent IPC, consisting of two 5-minute ischemia-reperfusion cycles (IPC group); 18 hearts underwent brief metabolic inhibition by exposure to two 5-minute infusions of 10 mmol/L sodium cyanide (CN group); and 15 hearts served as controls. " 09/12/1997 - "Cultured chick retina cells were submitted to 'chemical ischemia' by metabolic inhibition with sodium cyanide and iodoacetic acid, which block oxidative phosphorylation and glycolysis, respectively. " 06/01/2004 - "Overexpression of hsp10 by adenoviral infection decreased myocyte death induced by hydrogen peroxide, sodium cyanide, and simulated ischemia and reoxygenation (SI/RO). " 10/01/2012 - "For the ex vivo experiments, retinal eye cups were incubated with PBS or the chemical ischemia mixture [iodoacetic acid (5 mM)/sodium cyanide (25 mM)] in the absence or presence of SOM230 (10(-7)-10(-5) M) alone or in the presence of the sst(2) antagonist CYN-154806 (10(-7) or 10(-5) M). " 01/01/2003 - "By experiments of acute carbon-monoxide intoxication, acute nitrogen hypoxia and histotoxic hypoxia using sodium cyanide in cats, and by hemodynamic studies using plastic branch models, the following was elucidated; (1) severe tissue hypoxia, regardless of the underlying cause, and subsequent slight ischemia of the brain due to mild hypotension induce selective involvement of the cerebral white matter and pallidum, these two conditions being necessary and sufficient and this encephalopathy should be separately categorized as "hypoxic-ischemic encephalopathy" in hypoxic brain injuries, (2) the background of the selective involvement of these structures is an enormous development of the cerebrum in the brain, which induces thick white matter resulting in proper and long medullary artery, and especially small diameter ratio of the pallidal perforators to the middle cerebral artery, (3) the long course of the medullary artery produces the blood pressure drop in the deep white matter according to Hagen-Poiseuille's low, and according to that the smaller the diameter ratio, the larger the branching-loss coefficient (energy-loss co-efficient), smaller diameter ratio of the pallidal perforator, as compared with that of the putaminal perforator, induces more severe loss of the local blood flow selectively to the pallidum. "
5.	Asphyxia (Suffocation) 07/01/1987 - "Neuronal cortical cell cultures obtained from fetal mice were subjected to increasing concentrations of sodium cyanide (10-500 microM) for 6 days in order to simulate prolonged partial asphyxia. " 10/01/1999 - "Recording of phrenic efferent activity showed that the neural discharge increased in response to apneic asphyxia and sodium cyanide injections. " 10/01/1999 - "The changes in heart rate induced by the stimulation of arterial chemoreceptors by apneic asphyxia and left atrial - intracarotid injections of sodium cyanide were investigated in anesthetized artificially ventilated and paralysed monkeys. " 02/28/2006 - "At 3-4 months of age, two studies were performed to assess: (1) carotid sinus nerve responses to asphyxia and sodium cyanide in anesthetized rats and (2) ventilatory and blood gas responses in awake rats before (d0), during (d1 and d7), and 1 day following (d8) sustained hypoxia. " 03/01/1989 - "Fibres unresponsive to mechanical stimulation and asphyxia did not respond to sodium cyanide, dopamine or isoprenaline; some of these fibres were excited by nicotine. "

Related Drugs and Biologics

1.	Carbon Monoxide
2.	Chloralose
3.	Urethane (Ethyl Carbamate)
4.	Myoglobin
5.	Muscimol
6.	Isoflurane
7.	Oxygen
8.	Nitrogen
9.	Dithionite (Sodium Dithionite)
10.	Plastics

Related Therapies and Procedures

1.	Injections
2.	Intravenous Injections
3.	Intra-Arterial Injections
4.	Denervation
5.	Artificial Respiration (Mechanical Ventilation)