Nitroprusside serves as a source of nitric oxide, a potent peripheral vasodilator that affects both arterioles and venules (venules more than arterioles). Nitroprusside is often administered intravenously to patients who are experiencing a hypertensive emergency. [Wikipedia]
Indication
For immediate reduction of blood pressure of patients in hypertensive crises, reduce bleeding during surgery, and for the treatment of acute congestive heart failure
Pharmacology
Nitroprusside a powerful vasodilator relaxes the vascular smooth muscle and produce consequent dilatation of peripheral arteries and veins. Other smooth muscle (e.g., uterus, duodenum) is not affected. Sodium nitroprusside is more active on veins than on arteries.
Toxicity
Overdosage of nitroprusside can be manifested as excessive hypotension or cyanide toxicity or as thiocyanate toxicity. The acute intravenous mean lethal doses (LD50) of nitroprusside in rabbits, dogs, mice, and rats are 2.8, 5.0, 8.4, and 11.2 mg/kg, respectively.
Affected Organisms
Humans and other mammals
Biotransformation
Metabolized by reaction with hemoglobin to produce cyanmethemoglobin and cynide ions
Half Life
Approximately 2 minutes
Elimination
One molecule of sodium nitroprusside is metabolized by combination with hemoglobin to produce one molecule of cyanmethemoglobin and four CNˉ ions, thiosulfate reacts with cyanide to produce thiocyanate, thiocyanate is eliminated in the urine.