- 同
- Nipride
- 関
- Sodium nitroprusside
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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2016/01/22 04:15:59」(JST)
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Idealized depiction of this compound (top), and a picture of a sample (bottom).
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| Systematic (IUPAC) name | |
|---|---|
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disodium pentacyano(nitroso)irondiuide
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| Clinical data | |
| Trade names | Nipride, Nitropress |
| AHFS/Drugs.com | monograph |
| Licence data | US FDA:link |
| Pregnancy category |
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| Legal status |
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| Routes of administration |
Intravenous |
| Pharmacokinetic data | |
| Bioavailability | 100% (Intravenous) |
| Metabolism | By haemoglobin being converted to cyanmethaemoglobin and cyanide ions |
| Biological half-life | <2 minutes (3 days for thiocyanate metabolite) |
| Excretion | Renal (100%; as thiocyanate)[1] |
| Identifiers | |
| CAS Number | 13755-38-9 |
| ATC code | C02DD01 |
| PubChem | CID: 11953895 |
| DrugBank | DB00325 |
| ChemSpider | 21170789 |
| UNII | EAO03PE1TC |
| ChEMBL | CHEMBL136478 |
| Synonyms | SNP |
| Chemical data | |
| Formula | C5FeN6Na2O |
| Molecular mass | 261.918 |
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SMILES
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InChI
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| Physical data | |
| Density | 1.72 g/cm3 |
| Solubility in water | 100 mg/mL (20 °C) |
Sodium nitroprusside is an inorganic compound with the formula Na2[Fe(CN)5NO], usually encountered as the dihydrate, Na2[Fe(CN)5NO]·2H2O.[2] This red-colored sodium salt dissolves in water ethanol to give solutions containing the free complex dianion [Fe(CN)5NO]2−.
This compound is used as a drug. In this role it is abbreviated SNP, and it has tradenames like Nitropress. It acts as a drug by releasing nitric oxide; it belongs to the class of NO-releasing drugs as a result. This drug is used as a vasodilator to reduce blood pressure. Sodium nitroprusside is also used as an analytical reagent for the detection of methyl ketones, and for the detection of amines that are often found in illicit drugs.
It is on the WHO Model List of Essential Medicines, the most important medications needed in a basic health system.[3]
Contents
- 1 Medical use
- 2 Adverse effects
- 2.1 Contraindications
- 2.2 Interactions
- 2.3 Overdose
- 2.4 Toxicology
- 3 Mechanism of action
- 4 Structure and properties
- 5 Preparation
- 6 Analytical reagent
- 7 Other uses
- 8 References
Medical use
Sodium nitroprusside is primarily used as a vasodilator. It was first used in human medicine in 1928.[4] By 1955, data on its safety during short-term use in patients with severe hypertension had become available.[4] Despite this, due to difficulties in its chemical preparation, it was not finally approved by the US FDA until 1974 for the treatment of severe hypertension.[4] By 1993, its popularity had grown such that total sales in the US had totalled US$2 million.[4]
Sodium nitroprusside has potent vasodilating effects in arterioles and venules (arterioles more than venules, but this selectivity is much less marked than that of nitroglycerin, which acts preferentially at venous smooth muscle) as a result of its breakdown to nitric oxide (NO).[5][6][7] It is intravenously infused in cases of acute hypertensive crises.[5][8] Its therapeutic effects are usually seen within a few minutes.[1]
Nitric oxide reduces both total peripheral resistance and venous return, thus decreasing both preload and afterload. So, it can be used in severe congestive heart failure where this combination of effects can act to increase cardiac output. In situations where cardiac output is normal, the effect is to reduce blood pressure.[5][6] It is sometimes also used to induce hypotension (to reduce bleeding) for surgical procedures (for which it is also FDA, TGA, and MHRA labelled).[5][8][9]
This compound has also been successfully used as a treatment for aortic valve stenosis,[10] erythromelalgia,[11] oesophageal varices,[12] severe pyrexia (fever),[13] lactic acidosis,[14] myocardial infarction,[15] neuroleptic malignant syndrome,[16] pulmonary hypertension,[17][18][19] respiratory distress syndrome in the newborn,[20][21] shock,[21] cerebral vasospasm,[22][23] ergot toxicity,[24][25][26][27] and ventricular septal defects.[28]
Adverse effects
Adverse effects by incidence and severity[5][6][7]
Common
- Bradyarrhythmia (low heart rate)
- Hypotension (low blood pressure)
- Palpitations
- Tachyarrhythmia (high heart rate)
- Apprehension
- Restlessness
- Confusion
- Dizziness
- Headache
- Somnolence
- Rash
- Sweating
- Thyroid suppression
- Muscle twitch
- Oliguria
- Renal azotemia
Unknown frequency
- Nausea
- Retching
- Anxiety
- Chest discomfort
- Paraesthesial warmth
- Abdominal pain
- Orthostatic hypotension
- ECG changes
- Skin irritation
- Flushing
- Injection site erythema
- Injection site streaking
Serious
- Ileus
- Reduced platelet aggregation
- Haemorrhage
- Increased intracranial pressure
- Metabolic acidosis
- Methaemoglobinaemia
- Cyanide poisoning
- Thiocyanate toxicity
Contraindications
Sodium nitroprusside should not be used for compensatory hypertension (e.g. due to an anteriovenous stent or coarctation of the aorta).[6] It should not be used in patients with inadequate cerebral circulation or in patients who are near death. It should not be used in patients with vitamin B12 deficiency, anaemia, severe renal disease, or hypovolaemia.[6] Patients with conditions associated with a higher cyanide/thiocyanate ratio (e.g. congenital (Leber's) optic atrophy, tobacco amblyopia) should only be treated with sodium nitroprusside with great caution.[6] Its use in patients with acute congestive heart failure associated with reduced peripheral resistance is also not recommended.[6] Its use in hepatically impaired individuals is also not recommended, as is its use in cases of pre-existing hypothyroidism.[5]
Its use in pregnant women is advised against, although the available evidence suggests it may be safe, provided maternal pH and cyanide levels are closely monitored.[6][29] Some evidence suggests sodium nitroprusside use in critically ill children may be safe, even without monitoring of cyanide level.[30]
Interactions
The only known drug interactions are pharmacodynamic in nature, that is it is possible for other antihypertensive drugs to reduce the threshold for dangerous hypotensive effects to be seen.[6]
Overdose
Due to its cyanogenic nature, overdose may be particularly dangerous. Treatment of sodium nitroprusside overdose includes the following:[6][31]
- Discontinuing sodium nitroprusside administration
- Buffering the cyanide by using sodium nitrite to convert haemoglobin to methaemoglobin as much as the patient can safely tolerate
- Infusing sodium thiosulfate to convert the cyanide to thiocyanate.
Haemodialysis is ineffective for removing cyanide from the body but it can be used to remove most of the thiocyanate produced from the above procedure.[6]
Toxicology
The cyanide can be detoxified by reaction with a sulfur-donor such as thiosulfate, catalysed by the enzyme rhodanese.[32] In the absence of sufficient thiosulfate, cyanide ions can quickly reach toxic levels.[32]
| Species | LD50 (mg/kg) for oral administration[33] | LD50 (mg/kg) for IV administration[6] | LD50 (mg/kg) for skin administration[33] |
|---|---|---|---|
| Mouse | 43 | 8.4 | ? |
| Rat | 300 | 11.2 | >2000 |
| Rabbit | ? | 2.8 | ? |
| Dog | ? | 5 | ? |
Mechanism of action
Sodium nitroprusside breaks down in circulation to release nitric oxide (NO).[4] It does this by binding to oxyhaemoglobin to release cyanide, methaemoglobin and nitric oxide.[4] NO activates guanylate cyclase in vascular smooth muscle and increases intracellular production of cGMP. cGMP activates protein kinase G which activates phosphatases which inactivate myosin light chains.[34] Myosin light chains are involved in muscle contraction. The end result is vascular smooth muscle relaxation, which allow vessels to dilate.[34] This mechanism is similar to that of phosphodiesterase 5 (PDE5) inhibitors such as sildenafil (Viagra) and tadalafil (Cialis), which elevate cGMP concentration by inhibiting its degradation by PDE5.[35]
A role for NO in various common psychiatric disorders including schizophrenia,[36][37][38][39] bipolar disorder[40][41][42] and major depressive disorder[43][44][45] has been proposed and supported by several clinical findings. These findings may also implicate the potential of drugs that alter NO signalling such as SNP in their treatment.[38][44] Such a role is also supported by the findings of the recent SNP clinical trial[46] and other clinical trials that have demonstrated the efficacy of minocycline (a nitric oxide synthase inhibitor) in treating the negative and cognitive symptoms of schizophrenia.[47]
Structure and properties
Structure of sodium nitroprusside in the solid state, obtained by neutron diffraction
Nitroprusside is a complex anion that features an octahedral iron(II) centre surrounded by five tightly bound cyanide ligands and one linear nitric oxideligand (Fe-N-O angle = 176.2 °[48]). The anion possesses idealized C4vsymmetry.
Nitric oxide is a non-innocent ligand. Due to the linear Fe-N-O angle, the relatively short N-O distance of 113 pm[48] and the relatively high stretching frequency of 1947 cm−1, the complex is formulated as containing an NO+ ligand.[49] Consequently, iron is assigned an oxidation state of 2+. The iron center has a diamagnetic low-spin d6 electron configuration, although a paramagnetic long-lived metastable state has been observed by EPR spectroscopy.[50]
The chemical reactions of sodium nitroprusside are mainly associated with the NO ligand.[51] For example, addition of S2− ion to [Fe(CN)5(NO)]2− produces the red [Fe(CN)5(NOS)]4− ion, which is the basis for a sensitive test for S2− ions. An analogous reaction also exists with OH− ions, giving [Fe(CN)5(NO2)]4−.[49] Roussin's red salt (K2[Fe2S2(NO)4]) and Roussin's black salt (NaFe4S3(NO)7) are related iron nitrosyl complexes. The former was first prepared by treating nitroprusside with sulfur.[52]
This compound decomposes to sodium ferrous ferrocyanide, sodium ferrocyanide, nitric oxide, and cyanogen at about 450 °C. It decomposes in aqueous acid to liberate hydrocyanic acid (HCN).[53] Shielded from light, the concentrated solution is stable for more than two years at room temperature. It breaks down rapidly upon exposure to light, although the details are poorly understood. It degrades when heated (e.g. by sterilization in an autoclave), but addition of citric acid is helpful.[54]
Preparation
Sodium nitroprusside can be synthesized by digesting a solution of potassium ferrocyanide in water with nitric acid, followed by neutralization with sodium carbonate:[55]
- K4[Fe(CN)6] + 6 HNO3 → H2[Fe(CN)5(NO)] + CO2 + NH4NO3 + 4 KNO3
- H2[Fe(CN)5NO] + Na2CO3 → Na2[Fe(CN)5(NO)] + CO2 + H2O
Alternatively, ferrocyanide may be treated oxidized with nitrite as well:[49]
- [Fe(CN)6]4− + H2O + NO2− → [Fe(CN)5(NO)]2− + CN− + 2 OH−
Analytical reagent
Sodium nitroprusside was found by Legal to give a reaction with acetone or creatine under basic conditions in 1882. Rothera refined this method by the use of ammonia in place of sodium or potassium hydroxide. The reaction was now specific for methyl ketones. Addition of ammonium salts (e.g. ammonium sulfate) improved the sensitivity of the test, too.[56]
In this test, known as Rothera's test, methyl ketones (CH3C(=O)-) under alkaline conditions give bright red coloration (see also iodoform test). Rothera's test was initially applied to detecting ketonuria (a symptom of diabetes) in urine samples. This reaction is now exploited in the form of urine test strips (e.g. "Ketostix").[57]
Sodium nitroprusside is used in a separate urinalysis test known as the cyanide nitroprusside test or Brand's test. In this test, sodium cyanide is added first to urine and let stand for about 10 minutes. In this time, disulfide bonds will be broken by the released cyanide. The destruction of disulfide bonds liberates cysteine from cystine as well as homocysteine from homocystine. Next, sodium nitroprusside is added to the solution and it reacts with the newly freed sulfhydryl groups. The test will turn a red/purple colour if the test is positive, indicating significant amounts of amino acids were in the urine (aminoaciduria). Cysteine, cystine, homocysteine, and homocystine all react when present in the urine when this test is performed. This test can indicate inborn errors of amino acid transporters such as cystinuria, which results from pathology in the transport of dibasic amino acids.[58]
Sodium nitroprusside is also able to detect amines. This compound is thus used as a stain to indicate amines in thin layer chromatography.[59] Sodium nitroprusside is similarly used as a presumptive test for the presence of alkaloids (amine-containing natural products) common in illicit substances.[60] The test, called Simon's test, is performed by adding 1 volume of a solution of sodium nitroprusside and acetaldehyde in deionized water to a suspected drug, followed by the addition of 2 volumes of an aqueous sodium carbonate solution. The test turns blue for some secondary amines. The most common secondary amines encountered in forensic chemistry include 3,4-methylenedioxymethamphetamine (MDMA, the main component in Ecstasy) and phenethylamines such as methamphetamine. Sodium nitropruside is also useful in the identification the mercaptans (thiol groups) in the nitroprusside reaction.
Other uses
Sodium nitroprusside spectrum is used to calibrate Mössbauer spectrometers
Sodium nitroprusside is often used as a reference compound for the calibration of Mössbauer spectrometers.[53] Sodium nitroprusside crystals are also of interest for optical storage. For this application, sodium nitroprusside can be reversibly promoted to a metastable excited state by blue-green light, and de-excited by heat or red light.[61]
In physiology research, sodium nitroprusside is frequently used to test endothelium-independent vasodilation. Iontophoresis, for example, allows local administration of the drug, preventing the systemic effects listed above but still inducing local microvascular vasodilation. Sodium nitroprusside is also used in microbiology, where it has been linked with the dispersal of Pseudomonas aeruginosa biofilms by acting as a nitric oxide donor.[62][63]
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UpToDate Contents
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- 1. 高血圧緊急症の薬物治療 drug treatment of hypertensive emergencies
- 2. 急性非代償性心不全の治療：治療の要素 treatment of acute decompensated heart failure components of therapy
- 3. シアン化物中毒 cyanide poisoning
- 4. 高血圧緊急症の治療 treatment of specific hypertensive emergencies
- 5. 大動脈解離の管理 management of aortic dissection
English Journal
- Nitric oxide ameliorates zinc oxide nanoparticles-induced phytotoxicity in rice seedlings.
- Chen J1, Liu X2, Wang C3, Yin SS2, Li XL2, Hu WJ4, Simon M2, Shen ZJ2, Xiao Q5, Chu CC6, Peng XX7, Zheng HL8.
- Journal of hazardous materials.J Hazard Mater.2015 Oct 30;297:173-82. doi: 10.1016/j.jhazmat.2015.04.077. Epub 2015 Apr 29.
- Nitric oxide (NO) has been found to function in enhancing plant tolerance to various environmental stresses. However, role of NO in relieving zinc oxide nanoparticles (ZnO NPs)-induced phytotoxicity remains unknown. Here, sodium nitroprusside (SNP, a NO donor) was used to investigate the possible ro
- PMID 25958266
- Xanthan gum protects rabbit articular chondrocytes against sodium nitroprusside-induced apoptosis in vitro.
- Chen Q1, Mei X2, Han G3, Ling P4, Guo B2, Guo Y5, Shao H4, Wang G1, Cui Z2, Bai Y1, Xu F1.
- Carbohydrate polymers.Carbohydr Polym.2015 Oct 20;131:363-9. doi: 10.1016/j.carbpol.2015.06.004. Epub 2015 Jun 8.
- We have previously reported that intra-articular injection of xanthan gum (XG) could significantly ameliorate the degree of joint cartilage degradation and pain in experimental osteoarthritis (OA) model in vivo. In this present study, we evaluated the protective effect of XG against Sodium nitroprus
- PMID 26256195
- Nitric oxide influences potassium currents in inner hair cells isolated from guinea-pig cochlea.
- Kimitsuki T1.
- Auris, nasus, larynx.Auris Nasus Larynx.2015 Oct;42(5):360-4. doi: 10.1016/j.anl.2015.02.011. Epub 2015 Mar 10.
- OBJECTIVE: Nitric oxide (NO) is a diffusible second messenger, which regulates neurotransmission, serving as the principal endothelium-derived relaxing factor. NO also acts as an ion channel modulator. Nitric oxide synthase (NOS) has been identified in the inner ear, although its physiological role
- PMID 25769241
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