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Nitroprusside (Systemic)

Primary: CV402
Secondary: CV500; CV900; AD900

Commonly used brand name(s): Nipride; Nitropress.

Note: For a listing of dosage forms and brand names by country availability, see Dosage Forms section(s).



vasodilator, congestive heart failure—

myocardial infarction therapy adjunct—

antidote (to ergot alkaloid poisoning)—


Note: Bracketed information in the Indications section refers to uses that are not included in U.S. product labeling.


Congestive heart failure (treatment)1—Nitroprusside is indicated for the management of acute congestive heart failure {10}.

Hypertension (treatment)—Nitroprusside is indicated for the immediate reduction of blood pressure of patients in hypertensive crisis {08} {09}.
—For additional information on initial therapeutic guidelines related to the treatment of hypertension, see Appendix III.

Hypotension, controlled (induction and maintenance)—Nitroprusside is indicated for producing controlled hypotension during surgery to reduce bleeding into the surgical field {08} {09}.

[Hypertension, paroxysmal, in surgery for pheochromocytoma (treatment)]1—Nitroprusside is used to control paroxysmal hypertension prior to and during surgery for pheochromocytoma.

[Myocardial infarction (treatment adjunct)]1—Use of nitroprusside to reduce afterload is also recommended in patients with acute myocardial infarction who are hypertensive with persistent chest pain or left ventricular failure.

[Valvular regurgitation (treatment adjunct)]1—Nitroprusside is also used as an adjunct to standard treatment of aortic or mitral regurgitation prior to surgical intervention.

[Toxicity, ergot alkaloid (treatment) ]1—Nitroprusside is also used for treatment of peripheral vasospasm caused by ergot alkaloid overdose.

Acceptance not established
Studies and case reports suggest that nitroprusside may be used for the treatment of pulmonary hypertension in pediatric patients.{13}{14}{15}{16}{17}{18} However, data are insufficient to establish safety and efficacy of nitroprusside for this indication.{13}{14}{15}{16}{17}{18}

Nitroprusside should not be used in the treatment of compensatory hypertension (such as in arteriovenous shunt or coarctation of the aorta) {08} {09}.

1 Not included in Canadian product labeling.


Physicochemical characteristics:
Molecular weight—

Mechanism of action/Effect:

Antihypertensive—Hypertension or controlled hypotension: Causes vasodilation by a direct effect on arterial and venous smooth muscle, with no effect on uterine or duodenal smooth muscle or on myocardial contractility; regional distribution of blood flow is only marginally affected. Reduces peripheral resistance and has a variable effect on cardiac output {05} {08} {09}. Is more active on veins than arteries (but less markedly so than nitroglycerin) {08} {09}. Increases renin activity {08} {09}.

Vasodilator, congestive heart failure—Beneficial effects in congestive heart failure are due to decreased systemic resistance, preload and afterload reduction, and improved cardiac output. {10}

Myocardial infarction therapy adjunct—The effect of nitroprusside on ischemic myocardial areas is not totally known. It dilates coronary arteries {08} {09}. The medication reportedly reduces myocardial oxygen consumption and relieves persistent chest pain but has also been found to aggravate ischemia by redistributing blood flow away from ischemic myocardium.

Valvular regurgitation therapy adjunct—In the treatment of valvular regurgitation, nitroprusside reduces aortic and left ventricular impedance.

Antidote (to ergot alkaloid poisoning)—Causes vasodilation.

Other actions/effects:

Slightly increases heart rate {08} {09} {10}. Decreases platelet aggregation {08} {09}.


By intraerythrocytic reaction with hemoglobin to produce cyanmethemoglobin and cyanide ion {08} {09}. Exogenous cyanide is sequestered by erythrocyte methemoglobin as cyanmethemoglobin until intraerythrocytic methemoglobin is saturated {08} {09}. Some cyanide ion is eliminated from the body as expired hydrogen cyanide, but most is enzymatically converted to thiocyanate, which is eliminated in the urine {08} {09}; this reaction requires a hepatic mitochondrial enzyme, rhodanase (thiosulfate-cyanide sulfur transferase), and a sulfur donor, especially thiosulfate, cystine, and cysteine {08} {09}. Cyanide not removed by any of these methods binds to mitochondrial cytochromes and prevents oxidative metabolism {05} {08} {09}; cells either are forced to provide for their energy needs via anaerobic pathways, generating lactic acid {08} {09}, or die hypoxic deaths {05} {08} {09}.

Cyanide is normally found in serum and is derived from dietary substrates and tobacco smoke {08} {09}. Normal cyanide ion concentrations in packed erythrocytes are less than 1 micromole per liter (25 mg per liter); these concentrations are doubled in heavy smokers {08} {09}.

At healthy steady state, less than 1% of hemoglobin is in the form of methemoglobin {08} {09}. Nitroprusside metabolism leads to methemoglobin formation either through dissociation of cyanmethemoglobin formed in the original reaction of nitroprusside with hemoglobin or by direct oxidation of hemoglobin by the released nitroso group {08} {09}. A patient with normal red-cell mass and normal methemoglobin concentrations can buffer about 175 mcg of cyanide ion per kg of body weight (mcg/kg), corresponding to a little less than 500 mcg/kg of infused sodium nitroprusside {08} {09}.

Thiosulfate is a normal constituent of serum, produced by cysteine {08} {09}. Normal physiological concentrations of 0.1 millimole per liter (11 mg per liter) are approximately double in children and in adults who are not eating {08} {09}. When thiosulfate is being supplied only by normal physiologic mechanisms, conversion of cyanide ion to thiocyanate generally occurs at about 1 mcg/kg per minute {08} {09}. This rate of cyanide clearance corresponds to steady-state processing of a sodium nitroprusside infusion of slightly more than 2 mcg/kg per minute {08} {09}. Cyanide begins to accumulate when sodium nitroprusside infusions exceed this rate {08} {09}.


Nitroprusside—Circulatory: About 2 minutes {08} {09} {10}.

Thiosulfate—After intravenous infusion: About 20 minutes {08} {09} {10}.

Thiocyanate—About 3 days {08} {09} {10}; may be doubled or tripled in renal failure {08} {09} {10}.

Onset of action:

Hypotensive—Within 1 to 2 minutes after start of an adequate infusion {08} {09} {10}.

Time to peak effect:

Hypotensive—Almost immediate.

Duration of action:

Hypotensive—1 to 10 minutes after infusion is stopped {08} {09}.

    Thiocyanate and infused thiosulfate—Renal {08} {09}.

Precautions to Consider


Studies have not been done in either animals or humans {08} {09} {10}.


Adequate and well-controlled studies in humans have not been done {08} {09} {10}. Birth of a stillborn infant without any obvious anomalies was reported after one woman was given nitroprusside to control gestational hypertension; however, cyanide concentrations in the infant's liver were well below usual toxic levels and the mother demonstrated no cyanide toxicity {08} {09}.

Teratogenicity studies in laboratory animals have not been done {08} {09} {10}. In three studies in pregnant ewes, nitroprusside was shown to cross the placenta; fetal cyanide levels were dose-related to maternal levels; fatal cyanide levels could be produced in fetuses by using high rates of nitroprusside administration to the pregnant ewes {08} {09} {10}.

FDA Pregnancy Category C.


It is not known whether nitroprusside is excreted in breast milk {08} {09} {10}. Problems in humans have not been documented.


Appropriate studies on the relationship of age to the effects of nitroprusside have not been performed in the pediatric population. However, pediatrics-specific problems that would limit the usefulness of this medication in children are not expected.


Although appropriate studies on the relationship of age to the effects of nitroprusside have not been performed in the geriatric population, the elderly may be more sensitive to the hypotensive effects {03} {08} {09}. In addition, elderly patients are more likely to have age-related renal function impairment, which may require caution in patients receiving nitroprusside.

Drug interactions and/or related problems
The following drug interactions and/or related problems have been selected on the basis of their potential clinical significance (possible mechanism in parentheses where appropriate)—not necessarily inclusive (» = major clinical significance):

Note: Combinations containing any of the following medications, depending on the amount present, may also interact with this medication.

Dobutamine    (concurrent use with nitroprusside may result in a higher cardiac output and a lower pulmonary wedge pressure)

Hypotension-producing medications, other (see Appendix II )    (concurrent use may result in increased hypotensive effects {08} {09} which may be severe; dosage adjustment based on careful blood pressure monitoring is recommended)

Sympathomimetics    (hypotensive effects of nitroprusside may be reduced when it is used concurrently with sympathomimetics)

Laboratory value alterations
The following have been selected on the basis of their potential clinical significance (possible effect in parentheses where appropriate)—not necessarily inclusive (» = major clinical significance):

With physiology/laboratory test values
Bicarbonate concentrations, blood and
PCO 2 and
pH    (may be decreased, indicating metabolic acidosis, during cyanide toxicity; however, may not be present until an hour or more after toxic cyanide concentrations are reached {08} {09})

Cyanide, serum    (concentrations increased with excessive rate of nitroprusside infusion; except at low nitroprusside infusion rates [less than 2 mcg per kg of body weight (mcg/kg) per minute] or with brief use, concentrations produced are significant, potentially reaching toxic or lethal levels; venous blood appears bright red because of hyperoxemia {08} {09})

Lactate, arterial blood    (concentrations may be increased in overdose, indicating metabolic acidosis, during cyanide toxicity; however, may not be present until an hour or more after toxic cyanide concentrations are reached {08} {09})

Methemoglobin, blood    (concentrations may rarely be increased if amount of nitroprusside administered exceeds rate at which back-conversion of methemoglobin to hemoglobin can occur {08} {09}; blood appears chocolate brown, without color change on exposure to air {08} {09})

Oxygen, venous blood    (concentrations increased in cyanide toxicity {08} {09}; venous blood appears bright red {08} {09})

Thiocyanate, serum    (concentrations increased as a result of cyanide enzymatic reaction with thiosulfate {08} {09}; with prolonged infusions, the steady-state concentration is increased with increased infusion rate {08} {09})

Medical considerations/Contraindications
The medical considerations/contraindications included have been selected on the basis of their potential clinical significance (reasons given in parentheses where appropriate)— not necessarily inclusive (» = major clinical significance).

Risk-benefit should be considered when the following medical problems exist
Anemia—for use in producing controlled hypotension during anesthesia only; patient's capacity to compensate may be diminished{08}{09} ; should be corrected prior to use of nitroprusside{08}{09}
» Cerebrovascular{08}{09} or coronary artery insufficiency    (reduced tolerance of hypotension)

» Encephalopathy or other conditions where intracranial pressure is elevated    (intracranial pressure may be further increased; nitroprusside should be used only with extreme caution {08} {09})

» Hepatic function impairment{08}{09}    (hepatic enzyme is involved in metabolism of nitroprusside)

Hypothyroidism    (thiocyanate, one of the metabolic products of nitroprusside, inhibits both uptake and binding of iodine {05} {08} {09})

Hypovolemia—for use in producing controlled hypotension during anesthesia only; patient's capacity to compensate may be diminished{08}{09} ; should be corrected prior to use of nitroprusside{08}{09}
» Leber's hereditary optic atrophy or
» Tobacco amblyopia    (deficiency or absence of enzyme [rhodanase] needed for metabolism of nitroprusside {08} {09})

Pulmonary function impairment    (aggravation of hypoxemia)

» Renal function impairment    (reduced excretion of thiocyanate)

Sensitivity to nitroprusside{02}
» Vitamin B 12 deficiency    (related to metabolism)

Patient monitoring
The following may be especially important in patient monitoring (other tests may be warranted in some patients, depending on condition; » = major clinical significance):

Acid-base balance and
Oxygen concentrations, venous{08}{09}    (may indicate metabolic acidosis resulting from cyanide toxicity; however, because measurable effects may be delayed an hour or more after toxic cyanide concentrations are reached, these values should not be used to decide when to treat for cyanide toxicity {08} {09})

» Blood pressure determinations    (should be made continuously, either with a continually reinflated sphygmomanometer or, preferably, an intra-arterial pressure sensor {08} {09})

    (pulmonary artery diastolic or wedge pressure determinations may be required in patients with acute myocardial infarction {08} {09})

Cyanide concentrations, serum    (may be determined; however, not particularly useful because the cyanide assay is technically difficult and cyanide concentrations in body fluids other than packed red cells are difficult to interpret {08} {09})

Methemoglobin concentrations, blood    (recommended in patients who have received more than 10 mg of nitroprusside per kg of body weight and who exhibit signs of impaired oxygen delivery despite adequate cardiac output and adequate arterial pO 2 {08} {09})

Thiocyanate concentrations, serum{08}{09}    (recommended at daily intervals in patients receiving prolonged nitroprusside infusions at a rate greater than 3 mcg per kg of body weight [mcg/kg] per minute [1 mcg/kg per minute in anuric patients] {04} {06} {08} {09}; should not exceed 1 millimole per liter {08} {09})

For congestive heart failure
Invasive hemodynamic monitoring and
Urine output    (recommended to guide titration of infusion rate {10})

Side/Adverse Effects

Note: A severe rebound hypertension has been reported after discontinuation of an infusion used to produce controlled hypotension during surgery {07}.

The following side/adverse effects have been selected on the basis of their potential clinical significance (possible signs and symptoms in parentheses where appropriate)—not necessarily inclusive:

Those indicating need for medical attention
Signs and/or symptoms of excessively rapid fall in blood pressure (appear to be related to rate of administration rather than total dose)
Abdominal pain (stomach pain){08}{09}
dizziness {08}{09}
excessive sweating {08}{09}
headache {08}{09}
muscle twitching {08}{09}
nervousness or anxiety {08}{09}
restlessness {08}{09}
retching {08}{09}
tachycardia, reflex {08}{09}

Note: Excessive hypotension, sometimes to levels low enough to compromise perfusion of vital organs, may be produced by small transient excesses in the infusion rate {08} {09}. Excessively rapid decreases in blood pressure can lead to irreversible ischemic injuries or death if patients are not properly monitored {08} {09}.

Signs and/or symptoms of thiocyanate toxicity
blurred vision
loss of consciousness
nausea and vomiting
shortness of breath
tinnitus (ringing in ears)

Note: Mild neurotoxicity ( tinnitus, miosis, hyperreflexia) occurs at serum thiocyanate concentrations of 1 millimole per liter (60 mg per liter). Thiocyanate toxicity becomes life-threatening at serum concentrations of 200 mg per liter {08} {09}.

Signs and/or symptoms of cyanide toxicity
Absence of reflexes
distant heart sounds
imperceptible pulse
metabolic acidosis {08}{09}
pink color
very shallow breathing
widely dilated pupils

Note: Nitroprusside infusion rates greater than 2 mcg per kg of body weight (mcg/kg) per minute generate cyanide ion faster than the body can normally eliminate it (administration of thiosulfate greatly increases the body's capacity for cyanide elimination) {08} {09}. The capacity of methemoglobin to buffer cyanide is exhausted from about 500 mcg/kg of nitroprusside (the amount administered in less than an hour at a rate of 10 mcg/kg per minute) {08} {09}. Above this level, toxic effects of cyanide may be rapid, serious, and lethal {08} {09}.
Elevated cyanide concentrations, metabolic acidosis, and marked clinical deterioration have occasionally been reported in patients given infusions at recommended rates for only a few hours (in one case, for only 35 minutes) {08} {09}.

Incidence less frequent or rare
increased intracranial pressure{08}{09}
methemoglobinemia —concentrations greater than 10%
pain or redness at site of injection {08}{09}
skin rash {08}{09}

Note: Hypothyroidism—Thiocyanate interferes with iodine uptake by the thyroid {08} {09} {05}.
Methemoglobinemia is usually rare, because the back-conversion process returning methemoglobin to hemoglobin is normally rapid {08} {09}. Even in patients congenitally incapable of back-converting methemoglobin, a cumulative dose of 10 mg of nitroprusside per kg of body weight (mg/kg) (e.g., given at a rate of 10 mcg/kg per minute for 16 hours) would be required to produce 10% methemoglobinemia {08} {09}.

General Dosing Information
Nitroprusside should be administered only by intravenous infusion by means of an infusion pump, preferably a volumetric pump {08} {09}.

It is recommended that patients receiving nitroprusside be in a setting with available equipment and personnel to allow blood pressure to be monitored continuously {08} {09}.

Care should be taken to avoid extravasation because of possible irritation.

Larger than ordinary doses may be required for hypotensive anesthesia in young, vigorous males.

It is recommended that administration of nitroprusside be discontinued immediately if administration of 10 mcg (0.01 mg) (sodium nitroprusside dihydrate) per kg of body weight per minute for 10 minutes does not produce adequate reduction of blood pressure {08} {09}.

Concurrent administration of sodium thiosulfate (at 5 to 10 times the rate of sodium nitroprusside administration) may reduce the risk of cyanide toxicity by increasing the rate of cyanide conversion {08} {09}. However, it has not been extensively studied, and in one study appeared to potentiate nitroprusside's hypotensive effect {08} {09}. Caution is necessary to avoid prolonged or high doses of sodium nitroprusside with sodium thiosulfate, which could lead to thiocyanate toxicity and hypovolemia {08} {09}.

Apparent tolerance has occurred occasionally. Although a correlation between tachyphylaxis and concomitant cyanide toxicity has been proposed {05} {08} {09}, no correlation has been demonstrated {08} {09}.

For use in treatment of hypertension
It is recommended that oral antihypertensive therapy be instituted while the patient is receiving nitroprusside and that nitroprusside be withdrawn as soon as the patient has stabilized {08} {09}. Patients receiving concomitant antihypertensive medication require lower doses of nitroprusside {08} {09}.

For use in treatment of congestive heart failure
Addition of a potent inotropic medication such as dopamine or dobutamine may be useful when doses of nitroprusside that are effective in restoring pump function in left ventricular congestive heart failure cause excessive hypotension.

For treatment of adverse effects/overdose
For methemoglobinemia

   • Intravenous administration of methylene blue in a dose of 1 to 2 mg per kg of body weight (mg/kg) given over several minutes {08} {09}. Extreme caution is necessary in patients likely to have substantial amounts of cyanide bound to methemoglobin as cyanmethemoglobin {08} {09}.
For excessive hypotension

   • Slowing or discontinuation of infusion {08} {09}; symptoms disappear quickly (within 1 to 10 minutes) {08} {09}. Placement of the patient in the Trendelenberg position to maximize venous return may be helpful {08} {09}.
For thiocyanate toxicity

   • Hemodialysis; clearance rates during dialysis can approach the blood flow rate of the dialyzer {08} {09}.
For cyanide toxicity

   • Discontinuation of nitroprusside administration {08} {09}. Because metabolic acidosis may not be evident until more than an hour after the appearance of dangerous cyanide concentrations, laboratory test results should not be awaited; treatment should be initiated with reasonable suspicion of cyanide toxicity {06} {08} {09}.
   • Intravenous administration of sodium nitrite (as a 3% solution), in a dose of 4 to 6 mg/kg over 2 to 4 minutes {08} {09}. Sodium nitrite provides a buffer for cyanide by converting as much hemoglobin into methemoglobin as the patient can safely tolerate {08} {09}; this dose can be expected to convert about 10% of the patient's hemoglobin, and this level of methemoglobinemia is not associated with any known hazards {08} {09}. Sodium nitrite infusion may cause transient vasodilation and hypotension, which should be managed as necessary {08} {09}. Amyl nitrite inhalations may be used in environments where intravenous administration of sodium nitrite may be delayed {08} {09}.
   • Immediately following sodium nitrite infusion, intravenous infusion of sodium thiosulfate in a sufficient amount to convert the cyanide into thiocyanate {08} {09}. The recommended dose of sodium thiosulfate is 150 to 200 mg/kg; a typical adult dose is 50 mL of a 25% solution (sodium thiosulfate is also available as a 50% solution) {08} {09}. Thiocyanate concentrations will be raised in acutely cyanide-toxic patients, but not to a dangerous level {08} {09}.
   • Hemodialysis is not effective in removing cyanide {08} {09}.
   • If necessary, the nitrite/thiosulfate regimen may be repeated, at half the original doses, after 2 hours {08} {09}.

Parenteral Dosage Forms


Usual adult and adolescent dose
Intravenous infusion, initially, 0.3 mcg (0.0003 mg) (sodium nitroprusside dihydrate) per kg of body weight per minute {08} {09}, adjusted every few minutes {08} {09} according to response; usual dose is 3 mcg (0.003 mg) per kg of body weight per minute {08} {09}.

Note: Geriatric patients may be more sensitive to the usual adult dose of nitroprusside {08} {09}.

Usual adult prescribing limits
10 mcg (0.01 mg) per kg of body weight per minute for a maximum period of 10 minutes {08} {09}, or a total dose of 3.5 mg per kg of body weight (500 mcg [0.5 mg] per kg of body weight during short-term infusions such as in controlled hypotension during surgery). To keep the steady-state thiocyanate concentration below 1 millimole per liter, the rate of a prolonged infusion should be no more than 3 mcg per kg of body weight per minute {08} {09} (1 mcg per kg of body weight per minute in anuric patients {08} {09}).

Usual pediatric dose
See Usual adult and adolescent dose {08} {09}.

Size(s) usually available:

50 mg (sodium nitroprusside dihydrate) (Rx) [Nitropress][Generic]


50 mg (sodium nitroprusside dihydrate) (Rx) [Nipride]

Packaging and storage:
Store below 40 °C (104 °F), preferably between 15 and 30 °C (59 and 86 °F), unless otherwise specified by manufacturer. Protect from light.

Preparation of dosage form:
Nitroprusside is prepared for intravenous infusion by dissolving the contents of a 50-mg vial in 2.3 mL of 5% dextrose injection only and shaking gently to dissolve {08} {09} {10}. The reconstituted solution must be diluted further in 250 to 1000 mL of 5% dextrose injection to achieve the desired concentration and the container is wrapped in a supplied opaque sleeve, aluminum foil, or other opaque material to protect it from light (it is not necessary to wrap the infusion drip chamber or the tubing) {08} {09}.

Solutions of nitroprusside should be freshly prepared and any unused portion discarded. A freshly prepared solution has a slight brownish tint and should be discarded if the color is dark brown, orange, or blue {08} {09} {10}.

It is recommended that solutions of nitroprusside not be kept or used longer than 24 hours {08} {09}, unless otherwise specified by the manufacturer.

No other medications should be added to infusion fluid containing nitroprusside {08} {09} {10}.

Sodium nitroprusside solution is rapidly degraded by trace contaminants, often with resulting color changes {08} {09} {10}. A change in color to blue, green, or bright red indicates reaction of nitroprusside ion with another substance, and the solution must be replaced and discarded {08} {09} {10}.

Sodium nitroprusside solution is sensitive to certain wavelengths of light {08} {09} {10} and therefore must be protected from light. After preparation of the medication, the container should be promptly wrapped in the supplied opaque sleeve, aluminum foil, or other opaque material (it is not necessary to wrap the infusion drip chamber or the tubing) {08} {09} {10}.

Revised: 08/16/2000


Note: All references used in the development and earlier revisions of this monograph have not yet been incorporated into the computer database and, therefore, are not listed below. Citations for information not yet referenced in the monograph will be provided upon request.

  1. Nitropress package insert (Abbott—US), 3/87.
  1. Precautions included in all USP DI monographs, 1990 revision, per DID policy.
  1. Wood M, Hyman S, Wood AJJ. A clinical study of sensitivity to sodium nitroprusside during controlled hypotensive anesthesia in young and elderly patients. Anesth Analg 1987; 66: 132-6.
  1. Achrafi H. Action of nitroprusside in multidrug-resistant hypertension [letter]. Lancet 1989 Oct 7; 2: 867.
  1. Benitz WE, Malachowski N, Cohen RS, et al. Use of sodium nitroprusside in neonates: efficacy and safety. J Pediatr 1985 Jan; 106: 102-10.
  1. Cetnarowski AB, Conti DR. Nitroprusside toxicity and low-dose infusion [letter]. Ann Intern Med 1986 Jun; 104: 895-6.
  1. Fahmy NR. Nitroprusside vs. a nitroprusside-trimethaphan mixture for induced hypotension: hemodynamic effects and cyanide release. Clin Pharmacol Ther 1985 Mar; 37: 264-70.
  1. Nitropress package insert (Abbott—US), 9/90.
  1. Nipride package insert (Roche—US), 10/90.
  1. Nitropress package insert (Abbott—US), Rev 1/92, Rec 4/92.
  1. Kreye VAW. Sodium nitroprusside. In: Scriabine A, ed. Pharmacology of antihypertensive drugs. New York: Raven Press, 1980: 373-96.
  1. Gaskins JD, Holt RJ, Kessler C. Comparative review of intravenous nitroglycerin and nitroprusside sodium. Hosp Form 1982 Jul; 928-34.
  1. Panel consensus, 3/00.
  1. Palhares DB, Figueiredo CS, Moura AJ. Endotracheal inhalatory sodium nitroprusside in severly hypoxic newborns. J Perinat Med 1998; 26: p. 219-24.
  1. Benitz WE, Rhine WD, Van Meurs KP, et al. Nitrovasodilator therapy for severe respiratory distress syndrome. J Perinatol 1996 Nov-Dec; 16: p. 443-8.
  1. Przybylo HJ, Stevenson GW, Schanbacher P, et al. Sodium nitroprusside metabolism in children during hypothermic cardiopulmonary bypass. Anesth Analg 1995; 81(5): p. 952-6.
  1. Linakis JG, Lacouture PG, Woolf A. Monitoring cyanide and thiocyanate concentrations during infusion of sodium nitroprusside in children. Pediatr Cardiol 1991; 12(4): p. 214-8.
  1. Kunathai S, Sholler GF, Celermajer JM, et al. Nitroprusside in children after cardiopulmary bypass: a study of thiocyanate toxicity. Pediatr Cardiol 1989; 10(3): p. 121-4.

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