Sodium nitroprusside is a potent peripheral vasodilator which affects both arterioles and venules.

Indications

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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.

Mechanism of action

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Its mechanism of action appears to be liberation of nitric oxide (NO) as it is metabolised in the erythrocyte, converting Haemoglobin to cyanomethaemaglobin. Nitroprusside also releases cyanide ions which are converted in the liver to thiocyanate by the enzyme rhodanese, a reaction which requires a sulfur donor such as thiosulfate. 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 less than 10 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.

Role in research

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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.

Cyanides | Vasodilators | Nitroprussid