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Sodium nitroprusside (Na3Fe(CN)5NO) is a potent peripheral vasodilator which affects both arterioles and venules.
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.
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 rhodanase, 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.
Nitroprusside is light-sensitive, and breaks down in sunlight, producing cyanide.
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.
Despite its toxicity, nitroprusside is frequently used because it the only effective drug in certain clinical circumstances such as severe hypertension or for rapid control of blood pressure during vascular surgery and neurosurgery.
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