Sodium nitroprusside
Clinical data | |
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Trade names | Nipride, Nitropress, others |
Other names | SNP |
AHFS/Drugs.com | Monograph |
License data |
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Pregnancy category |
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Intravenous | |
ATC code | |
Legal status | |
Legal status | |
Pharmacokinetic data | |
Bioavailability | 100% (intravenous) |
Metabolism | By haemoglobin being converted to cyanmethaemoglobin and cyanide ions |
Onset of action | nearly immediate[3] |
Elimination half-life | <2 minutes (3 days for thiocyanate metabolite) |
Duration of action | 1 to 10 minutes[3] |
Excretion | kidney (100%; as thiocyanate)[4] |
Identifiers | |
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JSmol) | |
Density | 1.72 g/cm3 |
Solubility in water | 100 mg/mL (20 °C) |
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Sodium nitroprusside (SNP), sold under the brand name Nitropress among others, is a medication used to lower
It is available as a
Side effects and mechanism
Common side effects include
History, society and culture
Sodium nitroprusside was discovered as early as 1850 and found to be useful in medicine in 1928.[8][9] It is on the World Health Organization's List of Essential Medicines.[10][11] Sodium nitroprusside is light sensitive, so it needs to be shielded from light to prevent degradation.[12]
Medical use
Sodium nitroprusside is
Nitric oxide reduces both total peripheral resistance and venous return, thus decreasing both
The medication is extremely beneficial for use in medical patients because the effects of the medication will directly stop the second that it stops being infused. This is due to the metabolism of the drug, and the rapid inactivation to thiocyanate once conversion of the drug stops.
This compound has also been used as a treatment for
Adverse effects
Adverse effects by incidence and severity[13][15][26]
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 arteriovenous stent or coarctation of the aorta).[15] 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.[15] 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.[15] Its use in patients with acute congestive heart failure associated with reduced peripheral resistance is also not recommended.[15] Its use in hepatically impaired individuals is also not recommended, as is its use in cases of pre-existing hypothyroidism.[13]
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.[15][27] Some evidence suggests sodium nitroprusside use in critically ill children may be safe, even without monitoring of cyanide level.[28]
Interactions
The only known drug interactions are
Overdose
Due to its cyanogenic nature, overdose may be particularly dangerous. Treatment of sodium nitroprusside overdose includes the following:[15][29]
- 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.
Toxicology
The cyanide can be detoxified by reaction with a sulfur-donor such as thiosulfate, catalysed by the enzyme rhodanese.[30] In the absence of sufficient thiosulfate, cyanide ions can quickly reach toxic levels.[30] Hydroxocobalamin can be administered to reduce the risk of thiocyanate toxicity induced by nitroprusside.[31]
Species | LD50 (mg/kg) for oral administration[32] | LD50 (mg/kg) for IV administration[15] |
LD50 (mg/kg) for skin administration[32] |
---|---|---|---|
Mouse | 43 | 8.4 | ? |
Rat | 300 | 11.2 | >2000 |
Rabbit | ? | 2.8 | ? |
Dog | ? | 5 | ? |
Mechanism of action
As a result of its breakdown to nitric oxide (NO), sodium nitroprusside has potent
Sodium nitroprusside breaks down in circulation to release
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]
Structure and properties
Nitroprusside is an inorganic compound with the chemical formula Na2[Fe(CN)5NO], usually encountered as the dihydrate, Na2[Fe(CN)5NO]·2H2O.[47] This red-colored sodium salt dissolves in water or ethanol to give solutions containing the free complex dianion [Fe(CN)5NO]2−.
Nitroprusside is a complex
Due to the linear Fe-N-O angle, the relatively short N-O distance of 113 pm
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 violet colour [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]
Preparation
Sodium nitroprusside can be synthesized by digesting a solution of potassium ferrocyanide in water with nitric acid, followed by neutralization with sodium carbonate:[53]
Alternatively, the nitrosyl ligand can be introduced using nitrite:[49]
Other uses
Sodium nitroprusside is often used as a reference compound for the calibration of
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.[56][57]
Analytical reagent
Sodium nitroprusside is also used as an analytical reagent under the name sodium nitroferricyanide for the detection of methyl ketones, amines, and thiols. It is also used as a catalyst in the quantitative determination of ammonia in water samples via the phenate method.[58]
Ketones
The nitroprusside reaction is used for the identification of ketones in urine testing.[59] Sodium nitroprusside was found 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.[60]
In this test, known as Rothera's test, methyl ketones (CH3C(=O)-) under alkaline conditions give bright red coloration (see also
Thiols and cysteine
The nitroprusside reaction is a
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,
Amines
Sodium nitroprusside is also used to detect
History
Sodium nitroprusside is primarily used as a vasodilator. It was first used in human medicine in 1928.
References
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