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Sodium nitroprusside - Wikipedia, the free encyclopedia

Sodium nitroprusside

From Wikipedia, the free encyclopedia

Sodium nitroprusside
Sample of sodium nitroprusside
Sodium nitroprusside
IUPAC name Sodium pentacyanonitrosylferrate(III)
Other names Sodium nitroprusside
Sodium nitroferricyanide
Sodium pentacyanonitrosylferrate

SNP
Sodium nitroferricyanide(III) dihydrate
Sodium nitroprusside dihydrate

Identifiers
CAS number [13755-38-9]
PubChem 26256
DrugBank APRD01143
RTECS number LJ8750000
ATC code C02DD01
Properties
Molecular formula Na2[Fe(CN)5NO]·2H2O
Molar mass 297.95 g mol−1 (dihydrate)
Appearance red powder
Solubility in water good
Structure
Coordination
geometry
octahedral at Fe
Pharmacology
Routes of
administration
Intravenous
Metabolism Circulatory
Elimination
half-life
2 minutes (metabolites: several days)
Excretion Renal
Legal status


Prescription only

Pregnancy
category
C
Hazards
Main hazards Cyanide poisoning
R-phrases 25
S-phrases 45
Except where noted otherwise, data are given for
materials in their standard state
(at 25 °C, 100 kPa)

Infobox disclaimer and references

Sodium nitroprusside is the chemical compound with the formula Na2[Fe(CN)5NO]·2H2O.[1] This salt serves as a source of nitric oxide, a potent peripheral vasodilator that affects both arterioles and venules (venules more than arterioles). Sodium nitroprusside is often administered intravenously to patients who are experiencing a hypertensive emergency.

Contents

[edit] Chemistry

"Nitroprusside" is an anion that is usually available as the dihydrated disodium salt, Na2[Fe(CN)5NO]·2H2O. This red solid dissolves in water, and to a lesser extent in alcohol to give a solution containing the dianion [Fe(CN)5NO]2−. This metal nitrosyl complex is the active agent. In this anion, the iron is octahedral, surrounded by five tightly bound cyanide ligands and one linear nitric oxide ligand. When the linear nitrosyl ligand is assigned a single positive charge, the iron is assigned an oxidation state of 2+. This is a paramagnetic ion.[citation needed] Its chemical reactions have been studied intensively.[2]

[edit] Indications

It reduces both total peripheral resistance as well as venous return, thus decreasing both preload and afterload. For this reason, it can be used in severe cardiogenic 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.

Nitroprusside is light-sensitive, and breaks down in sunlight, producing cyanide.

Despite its toxicity, nitroprusside is still used because it remains an effective drug in certain clinical circumstances such as malignant hypertension or for rapid control of blood pressure during vascular surgery and neurosurgery.

Nitroprusside is contraindicated in patients with renal failure.

[edit] Mechanism of action

Its mechanism of action appears to be liberation of nitric oxide (NO), which causes relaxation of vascular smooth muscle. Nitroprusside also releases cyanide ions which are converted in the liver to thiocyanate by the enzyme rhodanase, a reaction which requires a sulfur donor such as thiosulfate. Alternatively, cyanide may react with methemoglobin to form cyanomethemoglobin. Thiocyanate is then excreted by the kidney. In the absence of sufficient thiosulfate, cyanide ions can quickly reach toxic levels. The half-life of nitroprusside is 1-2 minutes although thiocyanate has an excretion half life of several days. The duration of treatment should not exceed 72 hours and thiocyanate plasma concentrations should be monitored.

[edit] Role in research

Sodium nitroprusside (often abbreviated SNP) is frequently used in vascular research to test endothelium-independent vasodilation. One method of administering SNP is by iontophoresis. This allows local administration of the drug, preventing the systemic effects listed above but still causing local microvascular vasodilation. NO liberated from the SNP diffuses into the vascular smooth muscle causing relaxation and subsequent vasodilatation. This vasodilatation is quantified by various techniques. This role in the treatment of hypertension was first performed at the Cleveland Clinic. [3]


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