Cyanide nitroprusside causing

Sodium nitroprusside (SNP) is both a venous and an arterial vasodilator. An important part of its vasodilator action is caused by the release of nitric oxide (NO), similarly as for the organic nitrates. SNP can only be administered via the intravenous route. It is a rapidly and short acting vasodilator. It has been used in the treatment of hypertensive emergencies and in the management of myocardial ischaemia. In spite of its vasodilator action it hardly influences heart rate, in contrast to hydralazine and minoxidil. The dosage of SNP should not be higher than 3 pg/kg/min within 48 h, in order to avoid the rise of cyanide ions and thiocyanate in the blood. 

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.]... 

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. 

The drug must be administered as a controlled continuous infusion, and the patient must be closely observed. Most hypertensive patients respond to an infusion of 0.25-1.5 flg/kg/min. Higher infusion rates are needed to produce controlled hypotension in normotensive patients under surgical anesthesia. Infusion of nitroprusside at rates >5 flg/kg/min over a prolonged period can cause cyanide and/or thiocyanate poisoning. Patients receiving other antihypertensive medications usually require less nitroprusside to lower blood pressure. If infusion rates of 10 pg/kg/min do not produce adequate reduction of blood pressure within 10 minutes, the rate of administration of nitroprusside should be reduced to minimize potential toxicity. 

Nitroprusside (Nipride) Converted to nitric oxide, which induces cGMP. cGMP stimulates a phosphorylation/ dephosphorylation cascade. Ultimately dephosphorylates myosin, causing smooth muscle relaxation. Continuous intravenous infusion used in hypertensive crisis. Severe hypotension, cyanide toxicity, hepatotoxicity. 

Cyanide-nutrient interactions are reported for alanine, which appears to exacerbate cyanide toxicity, and for cystine, which seems to alleviate toxicity. Dietary cyanide - at levels that do not cause growth depression -alleviates selenium toxicity in chickens, but not the reverse. For example, dietary selenium, as selenite, at lO.Omg/kg for 24 days, reduced growth, food intake, and food utilization efficiency, and produced increased liver size and elevated selenium residues the addition of 45.0 mg CN/kg diet (100.0 mg sodium nitroprusside/kg) eliminated all effects except elevated selenium residues in liver. The mechanism of alleviation is unknown and may involve a reduction of tissue selenium through selenocyanate formation, or increased elimination of excess selenium by increasing the amount of dimethyl selenide exhaled. At dietary levels of 135.0 mg CN/kg plus 10.0 mg selenium/kg chick growth was significantly decreased. This interaction can be lost if there is a deficiency of certain micronutrients or an excess of vitamin K. 

Excessively rapid infusion causes sweating, nausea, vomiting, anxiety, restlessness and muscle twitching these symptoms disappear after slowing down the infusion (146, 147, 148 ). The serious toxic effects of nitroprusside are a result of its metabolism. Nitroprusside is converted into cyanogen and cyanide and then further in thiocyanate in this system, cyanide and thiocyanate form a dynamic equilibrium. Thiocyanate is excreted mainly in the urine, with a half-life of about a week. 

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