Cyanide poisoning sodium nitroprusside

Although its mode is uncertain, sodium nitroprusside (SNP) is one of the most valuable vasodilators. Its use in clinical practice is suspect as the cyano-ligands render cyanide poisoning a possibility. However for ex vivo experiments this consideration is less important but the possibility of some biological action due to these ions remains. The mechanism by which SNP acts as a vasodilator is not fully understood. With the discovery of a physiological role for NO there has been renewed interest in mechanistic studies of reactions involving SNP and a re-examination of studies of SNP undertaken before 1987. So far, only one simple reaction leading to the release... 

Hydrogen cyanide (HCN) is a colorless, rapidly acting, highly poisonous gas or liquid that has an odor of bitter almonds. Most HCN is used as an intermediate at the site of production. Major uses include the manufacture of nylons, plastics, and fumigants. Exposures to HCN may occur in industrial situations as well as from cigarette smoke, combustion products, and naturally occurring cyanide compounds in foods. Sodium nitroprusside (Na2[Fe(CN)5 N0]-2H20), which has been used as an antihypertensive in humans, breaks down into nonionized HCN. 

Poisoning with cyanide may occur in a variety of ways accidental or intentional poisoning with cyanide salts, which are used in industry or in laboratories as a result of exposure to hydrogen cyanide in fires when polyurethane foam burns from sodium nitroprusside, which is used therapeutically as a muscle relaxant and produces cyanide as an intermediate product and from the natural product amygdalin, which is found in apricot stones, for example. 

Nitroprusside [nye troe PRUSS ide] is administered intravenously, and causes prompt vasodilation, with reflex tachycardia. It is capable of reducing blood pressure in all patients, regardless of the cause of hypertension. The drug has little effect outside the vascular system, acting equally on arterial and venous smooth muscle. [Note Because nitroprusside also acts on the veins, it can reduce cardiac preload.] Nitroprusside is metabolized rapidly (t1/2 of minutes) and requires continuous infusion to maintain its hypotensive action. Sodium nitroprusside exerts few adverse effects except for those of hypotension caused by overdose. Nitroprusside metabolism results in cyanide ion production, although cyanide toxicity is rare and can be effectively treated with an infusion of sodium thiosulfate to produce thiocyanate, which is less toxic and is eliminated by the kidneys (Figure 19.14). [Note Nitroprusside is poisonous if given orally because of its hydrolysis to cyanide.]... 

Cyanide. In contrast to [Fe(CN)6]4 , the [Fe(CN)6]3 ion is quite poisonous for kinetic reasons the latter dissociates and reacts rapidly, whereas the former is not labile. There is a variety of substituted ions [Fe(CN)3X]" (X= H20, N02, etc.), of which the best known is the nitroprusside ion [Fe(CN)5NO]2. Crystalline sodium nitroprusside dihydrate exhibits extremely long-lived electronic excited states.47 A metastable state I and a metastable state II have lifetimes greater than 104 s at temperatures below 185 and 140 K, respectively. The nitroprusside anion is attacked by OH to give [Fe(CN)5N02]2-. 

An ethical drug that may also cause cyanide poisoning in overdose is the potent vascular smooth-muscle relaxant sodium nitroprusside. Although nitroprusside is related chemically to ferricyanide, unlike the latter it penetrates into erythrocytes and reacts with hemoglobin to release its cyanide (Smith and Kruszyna, 1974). Fortunately, the therapeutic margin for nitroprusside appears to be quite large. 

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