Nitroferricyanide
Nitroferricyanide Uses, Dosage, Side Effects, Food Interaction and all others data.
Nitroferricyanide serves as a source of nitric oxide, a potent peripheral vasodilator that affects both arterioles and venules (venules more than arterioles). Nitroferricyanide is often administered intravenously to patients who are experiencing a hypertensive emergency.
Nitroferricyanide 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.
| Trade Name | Nitroferricyanide |
| Availability | Prescription only |
| Generic | Nitroprusside |
| Nitroprusside Other Names | Nitroferricyanide |
| Related Drugs | amlodipine, lisinopril, metoprolol, furosemide, carvedilol, spironolactone, hydralazine, nifedipine, captopril, enalapril |
| Type | |
| Formula | C5FeN6O |
| Weight | Average: 215.938 Monoisotopic: 215.948300785 |
| Groups | Approved, Investigational |
| Therapeutic Class | |
| Manufacturer | |
| Available Country | |
| Last Updated: | September 19, 2023 at 7:00 am |
Uses
Nitroferricyanide is a direct acting vasodilator used to treat hypertension, to induce controlled hypotension to reduce postoperative bleeding, and to manage acute heart failure.
For immediate reduction of blood pressure of patients in hypertensive crises, reduce bleeding during surgery, and for the treatment of acute congestive heart failure
Nitroferricyanide is also used to associated treatment for these conditions: Bleeding, Congestive Heart Failure (CHF), Hypertensive crisis
How Nitroferricyanide works
One molecule of sodium nitroprusside is metabolized by combination with hemoglobin to produce one molecule of cyanmethemoglobin and four CN- ions; methemoglobin, obtained from hemoglobin, can sequester cyanide as cyanmethemoglobin; thiosulfate reacts with cyanide to produce thiocyanate; thiocyanate is eliminated in the urine; cyanide not otherwise removed binds to cytochromes. Cyanide ion is normally found in serum; it is derived from dietary substrates and from tobacco smoke. Cyanide binds avidly (but reversibly) to ferric ion (Fe+++), most body stores of which are found in erythrocyte methemoglobin (metHgb) and in mitochondrial cytochromes. When CN is infused or generated within the bloodstream, essentially all of it is bound to methemoglobin until intraerythrocytic methemoglobin has been saturated.
Sodium nitroprusside is further broken down in the circulation to release nitric oxide (NO), which activates guanylate cyclase in the vascular smooth muscle. This leads to increased production of intracellular cGMP, which stimulates calcium ion movement from the cytoplasm to the endoplasmic reticulum, reducing the level of available calcium ions that can bind to calmodulin. This ultimately results in vascular smooth muscle relaxation and vessel dilation.
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.
Food Interaction
No interactions found.Nitroferricyanide Drug Interaction
Moderate: meperidine, haloperidol, dexmedetomidineMinor: diltiazemUnknown: aspirin, RHO Immunoglobulin , mycophenolate mofetil, sulfamethoxazole / trimethoprim, warfarin, apixaban, gentamicin, heparin, furosemide, levofloxacin, norepinephrine, enoxaparin, insulin isophane, acetaminophen, clopidogrel, midazolam
Nitroferricyanide Disease Interaction
Major: cerebral vascular insufficiency, compensatory hypertension, congenital optic atrophy, sepsisModerate: anemia, hepatic impairment, intracranial hypertension
Half Life
Approximately 2 minutes
Elimination Route
One molecule of sodium nitroprusside is metabolized by combination with hemoglobin to produce one molecule of cyanmethemoglobin and four CN¯ ions, thiosulfate reacts with cyanide to produce thiocyanate, thiocyanate is eliminated in the urine.
Innovators Monograph
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