Vasopressin (medication)

Last updated
Vasopressin
Vasopressin labeled.png
Arginine vasopressin3d.png
Clinical data
Pronunciation /ˌveɪzoʊˈprɛsɪn/
Trade names Vasostrict (USA), Reverpleg (FR), Empressin (GER), others
Other namesarginine vasopressin; argipressin
AHFS/Drugs.com Monograph
License data
Pregnancy
category
Routes of
administration 		Intravenous (IV), intramuscular (IM), subcutaneous (SC)
ATC code
Physiological data
Source tissues Supraoptic nucleus; Paraventricular nucleus of hypothalamus
Target tissuesSystem-wide
Receptors V1A, V1B, V2, OXTR
Agonists Felypressin, Desmopressin
Antagonists Diuretics
Metabolism Predominantly in the liver and kidneys
Legal status
Legal status
  • AU: S4 (Prescription only)
  • UK: POM (Prescription only)
  • US: ℞-only
Pharmacokinetic data
Protein binding 1%
Metabolism Predominantly in the liver and kidneys
Elimination half-life 10-20 minutes
Excretion Urine
Identifiers
  • 1-{[(4R,7S,10S,13S,16S,19R)-19-Amino-7-(2-amino-2-oxoethyl)-10-(3-amino-3-oxopropyl)-13-benzyl-16-(4-hydroxybenzyl)-6,9,12,15,18-pentaoxo-1,2-dithia-5,8,11,14,17-pentaazacycloicosan-4-yl]carbonyl}-L-p rolyl-L-arginylglycinamide
CAS Number
PubChem CID
IUPHAR/BPS
DrugBank
ChemSpider
UNII
KEGG
ChEBI
ChEMBL
CompTox Dashboard (EPA)
ECHA InfoCard 100.003.669 OOjs UI icon edit-ltr-progressive.svg
Chemical and physical data
Formula C46H65N15O12S2
Molar mass 1084.24 g·mol−1
3D model (JSmol)
Density 1.6±0.1 g/cm3
  • c1ccc(cc1)C[C@H]2C(=O)N[C@H](C(=O)N[C@H](C(=O)N[C@@H](CSSC[C@@H](C(=O)N[C@H](C(=O)N2)Cc3ccc(cc3)O)N)C(=O)N4CCC[C@H]4C(=O)N[C@@H](CCCN=C(N)N)C(=O)NCC(=O)N)CC(=O)N)CCC(=O)N
  • InChI=1S/C46H65N15O12S2 /c47-27-22-74-75-23-33(45(73)61-17-5-9-34(61)44(72)56-28(8-4-16-53-46(51)52)39(67)54-21-37(50)65)60-43(71)32(20-36(49)64)59-40(68)29(14-15-35(48)63)55-41(69)31(18-24-6-2-1-3-7-24)58-42(70)30(57-38(27)66)19-25-10-12-26(62)13-11-25/h1-3,6-7,10-13,27-34,62H,4-5,8-9,14-23,47H2,(H2,48,63)(H2,49,64)(H2,50,65)(H,54,67)(H,55,69)(H,56,72)(H,57,66)(H,58,70)(H,59,68)(H,60,71)(H4,51,52,53)/t27-,28-,29-,30-,31-,32-,33-,34-/m0/s1 Yes check.svgY
  • Key:KBZOIRJILGZLEJ-LGYYRGKSSA-N Yes check.svgY

Vasopressin infusions are in use for septic shock patients not responding to fluid resuscitation or infusions of catecholamines (e.g., dopamine or norepinephrine) to increase the blood pressure while sparing the use of catecholamines. These argipressins have much shorter elimination half-life (around 20 minutes) than synthetic non-arginine vasopresines with much longer elimination half-life of many hours. Further, argipressins act on V1a, V1b, and V2 receptors which consequently lead to higher eGFR and lower vascular resistance in the lungs. A number of injectable arginine vasopressins are in clinical use in the United States and the European Union. Pitressin among others, is a medication most commonly used in the treatment of frequent urination, increased thirst, and dehydration such as that resulting from diabetes insipidus, which causes increased and diluted urine. [2] [3] It is used to treat abdominal distension following some surgeries, and in stomach roentgenography. [3] Vasopressin is a hormone that affects the kidneys and reduces urine flow. [4]

Contents

Side effects may include stomach ache, vertigo, pale skin, flatulence, headache, or tremor. [3] [4]

It is available as a generic medication. [5]

Medical uses

Vasopressin is used to manage anti-diuretic hormone deficiency. It has off-label uses and is used in the treatment of gastrointestinal bleeding, ventricular tachycardia and ventricular defibrillation. Vasopressin is used to treat diabetes insipidus related to low levels of antidiuretic hormone. It is available as Pressyn. [6]

Vasopressin agonists are used therapeutically in various conditions, and its long-acting synthetic analogue desmopressin is used in conditions featuring low vasopressin secretion, as well as for control of bleeding (in some forms of von Willebrand disease and in mild haemophilia A) and in extreme cases of bedwetting by children. Terlipressin and related analogues are used as vasoconstrictors in certain conditions. Use of vasopressin analogues for esophageal varices commenced in 1970. [7]

Vasopressin infusions are also used as second line therapy in septic shock patients not responding to fluid resuscitation or infusions of catecholamines (e.g., dopamine or norepinephrine).

Catecholamine refractory hypotension in septic shock

Efficacy of vasopressin on systemic hemodynamics in catecholamine-resistant septic and postcardiotomy shock have been studied and published first in 2001 [8] Later, the group concluded the ischemic skin lesions (ISL) developed in patients with catecholamine-resistant vasodilatory shock have multi-factorial cause and shall not necessarily been seen a side effect of AVP solely. The presence of septic shock and a history of peripheral arterial occlusive disease are independent risk factors for the development of ISL. [9] In the last decade, in early hyperdynamic septic shock, the administration of high-dose AVP as a single agent proved to fail to increase mean arterial pressure in the first hour but maintains it above 70mmHg in two-thirds of patients at 48h. AVP decreases NE exposure, has no effect on the PrCO(2) - PaCO(2 )difference, and improves renal function and SOFA score. [10] This led to development of a large trial to see theeffect of arginin vasopressin as add-on to norepinephrine in septic shock. [11] It could be shown, if giving vasopressin in early stage of septic shock (norepinephrin < 15 microgramm/min and lactate < 1.4 mmol/L) there is a statistically significant interaction between vasopressin and corticosteroids. The combination of low-dose vasopressin and corticosteroids was associated with decreased 28 and 90 days mortality and organ dysfunction compared with norepinephrine and corticosteroids. [12]

2018 Surviving Sepsis Campaign Guidelines

The Surviving Sepsis Campaign guidelines recommend the very early management of the sepsis focusing on the hour-1 bundle. This includes use of Vasopressin 0.03 units/minute as add-on to norepinephrine (NE) with intent of either raising the mean arterial pressure or decreasing the norepinephrine dosage (i.e. de-catecholaminization). [13]

Cardiac arrest

Modern interest in vasopressors as a treatment for cardiac arrest stem mostly from canine studies performed in the 1960s by anesthesiologists Dr. John W. Pearson and Dr. Joseph Stafford Redding in which they demonstrated improved outcomes with the use of adjunct intracardiac epinephrine injection during resuscitation attempts after induced cardiac arrest. [14] Also contributing to the idea that vasopressors may be useful treatments in cardiac arrest are studies performed in the early to mid 1990s that found significantly higher levels of endogenous serum vasopressin in adults after successful resuscitation from out-of-hospital cardiac arrest compared to those who did not live. [15] [16] Results of animal models have supported the use of either vasopressin or epinephrine in cardiac arrest resuscitation attempts, showing improved coronary perfusion pressure [17] and overall improvement in short-term survival as well as neurological outcomes. [18]

Vasopressin vs. epinephrine

Although both vasopressors, vasopressin and epinephrine differ in that vasopressin does not have direct effects on cardiac contractility as epinephrine does. [18] Thus, vasopressin is theorized to be of increased benefit over epinephrine in cardiac arrest due to its properties of not increasing myocardial and cerebral oxygen demands. [18] This idea has led to the advent of several studies searching for the presence of a clinical difference in benefit of these two treatment choices. Initial small studies demonstrated improved outcomes with vasopressin in comparison to epinephrine. [19] However, subsequent studies have not all been in agreement. Several randomized controlled trials have been unable to reproduce positive results with vasopressin treatment in both return of spontaneous circulation (ROSC) and survival to hospital discharge, [19] [20] [21] [22] including a systematic review and meta-analysis completed in 2005 that found no evidence of a significant difference with vasopressin in five studied outcomes. [17]

Vasopressin and epinephrine vs. epinephrine alone

There is no current evidence of significant survival benefit with improved neurological outcomes in patients given combinations of both epinephrine and vasopressin during cardiac arrest. [17] [20] [23] [24] A systematic review from 2008 did, however, find one study that showed a statistically significant improvement in ROSC and survival to hospital discharge with this combination treatment; unfortunately, those patients that survived to hospital discharge had overall poor outcomes and many sustained permanent, severe neurological damage. [22] [24] A more recently published clinical trial out of Singapore has shown similar results, finding combination treatment to only improve the rate of survival to hospital admission, especially in the subgroup analysis of patients with longer "collapse to emergency department" arrival times of 15 to 45 minutes. [25]

Surgery for congenital heart disease

Vasopressin is used in managing hemodynamic instability in newborns and older children recovering from cardiac surgery. [26] [27] [28] [29] [30] [31] There is evidence that some children recovering from cardiac surgery have relative vasopressin deficiency, such that their endogenous plasma concentrations of arginine vasopressin are lower than what would be expected in this clinical setting. [27] [28] [31] Though low endogenous vasopressin concentrations in and of themselves do not cause hemodynamic instability, neonates and children recovering from cardiac surgery who develop hemodynamic instability and have low endogenous vasopressin concentrations are optimal candidates for this surgery. Unfortunately, measurement of endogenous vasopressin concentration is time-consuming and cumbersome, and not practical for bedside application. Copeptin, a more stable and easily measured product of pro-AVP processing, may be a means of identifying patients with low endogenous vasopressin concentrations. [28] Further research is needed. Also, systemic corticosteroids have been shown to suppress endogenous vasopressin production and release. [31] Neonates and children recovering from cardiac surgery who are receiving systemic corticosteroid therapy may also be optimal candidates for vasopressin therapy should hemodynamic instability be present.

Vasopressin receptor inhibition

A vasopressin receptor antagonist is an agent that interferes with action at the vasopressin receptors. They can be used in the treatment of hyponatremia. [32]

Related Research Articles

<span class="mw-page-title-main">Cardiac arrest</span> Sudden stop in effective blood flow due to the failure of the heart to beat

Cardiac arrest, also known as sudden cardiac arrest, is when the heart suddenly and unexpectedly stops beating. As a result blood will not be pumped around the body in normal circulation, consciousness will be rapidly lost, and breathing will be abnormal or absent. Without immediate intervention such as cardiopulmonary resuscitation (CPR), and possibly defibrillation, death will occur within minutes.

Clinical death is the medical term for cessation of blood circulation and breathing, the two criteria necessary to sustain the lives of human beings and of many other organisms. It occurs when the heart stops beating in a regular rhythm, a condition called cardiac arrest. The term is also sometimes used in resuscitation research.

<span class="mw-page-title-main">Shock (circulatory)</span> Medical condition of insufficient blood flow

Shock is the state of insufficient blood flow to the tissues of the body as a result of problems with the circulatory system. Initial symptoms of shock may include weakness, fast heart rate, fast breathing, sweating, anxiety, and increased thirst. This may be followed by confusion, unconsciousness, or cardiac arrest, as complications worsen.

<span class="mw-page-title-main">Sepsis</span> Life-threatening organ dysfunction triggered by infection

Sepsis is a potentially life-threatening condition that arises when the body's response to infection causes injury to its own tissues and organs.

<span class="mw-page-title-main">Vasopressin</span> Mammalian hormone released from the pituitary gland

Human vasopressin, also called antidiuretic hormone (ADH), arginine vasopressin (AVP) or argipressin, is a hormone synthesized from the AVP gene as a peptide prohormone in neurons in the hypothalamus, and is converted to AVP. It then travels down the axon terminating in the posterior pituitary, and is released from vesicles into the circulation in response to extracellular fluid hypertonicity (hyperosmolality). AVP has two primary functions. First, it increases the amount of solute-free water reabsorbed back into the circulation from the filtrate in the kidney tubules of the nephrons. Second, AVP constricts arterioles, which increases peripheral vascular resistance and raises arterial blood pressure.

<span class="mw-page-title-main">Septic shock</span> Dangerously low blood pressure due to damage from an organ infection

Septic shock is a potentially fatal medical condition that occurs when sepsis, which is organ injury or damage in response to infection, leads to dangerously low blood pressure and abnormalities in cellular metabolism. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) defines septic shock as a subset of sepsis in which particularly profound circulatory, cellular, and metabolic abnormalities are associated with a greater risk of mortality than with sepsis alone. Patients with septic shock can be clinically identified by requiring a vasopressor to maintain a mean arterial pressure of 65 mm Hg or greater and having serum lactate level greater than 2 mmol/L (>18 mg/dL) in the absence of hypovolemia. This combination is associated with hospital mortality rates greater than 40%.

<span class="mw-page-title-main">Neurogenic shock</span> Insufficient blood flow due to autonomic nervous system damage

Neurogenic shock is a distributive type of shock resulting in hypotension, often with bradycardia, caused by disruption of autonomic nervous system pathways. It can occur after damage to the central nervous system, such as spinal cord injury and traumatic brain injury. Low blood pressure occurs due to decreased systemic vascular resistance resulting from loss of sympathetic tone, which in turn causes blood pooling within the extremities rather than being available to circulate throughout the body. The slowed heart rate results from a vagal response unopposed by a sympathetic nervous system (SNS) response. Such cardiovascular instability is exacerbated by hypoxia, or treatment with endotracheal or endobronchial suction used to prevent pulmonary aspiration.

<span class="mw-page-title-main">Bupivacaine</span> Local anaesthetic drug

Bupivacaine, marketed under the brand name Marcaine among others, is a medication used to decrease feeling in a specific area. In nerve blocks, it is injected around a nerve that supplies the area, or into the spinal canal's epidural space. It is available mixed with a small amount of epinephrine to increase the duration of its action. It typically begins working within 15 minutes and lasts for 2 to 8 hours.

<span class="mw-page-title-main">Aminophylline</span> Chemical compound

Aminophylline is a compound of the bronchodilator theophylline with ethylenediamine in 2:1 ratio. The ethylenediamine improves solubility, and the aminophylline is usually found as a dihydrate.

<span class="mw-page-title-main">Dobutamine</span> Medication which strengthens heart contractions

Dobutamine is a medication used in the treatment of cardiogenic shock and severe heart failure. It may also be used in certain types of cardiac stress tests. It is given by IV only, as an injection into a vein or intraosseous as a continuous infusion. The amount of medication needs to be adjusted to the desired effect. Onset of effects is generally seen within 2 minutes. It has a half-life of two minutes. This drug is generally only administered short term, although it may be used for longer periods to relieve symptoms of heart failure in patients awaiting heart transplantation.

Distributive shock is a medical condition in which abnormal distribution of blood flow in the smallest blood vessels results in inadequate supply of blood to the body's tissues and organs. It is one of four categories of shock, a condition where there is not enough oxygen-carrying blood to meet the metabolic needs of the cells which make up the body's tissues and organs. Distributive shock is different from the other three categories of shock in that it occurs even though the output of the heart is at or above a normal level. The most common cause is sepsis leading to a type of distributive shock called septic shock, a condition that can be fatal.

Early goal-directed therapy was introduced by Emanuel P. Rivers in The New England Journal of Medicine in 2001 and is a technique used in critical care medicine involving intensive monitoring and aggressive management of perioperative hemodynamics in patients with a high risk of morbidity and mortality. In cardiac surgery, goal-directed therapy has proved effective when commenced after surgery. The combination of GDT and Point-of-Care Testing has demonstrated a marked decrease in mortality for patients undergoing congenital heart surgery. Furthermore, a reduction in morbidity and mortality has been associated with GDT techniques when used in conjunction with an electronic medical record.

<span class="mw-page-title-main">Dopexamine</span> Chemical compound

Dopexamine is a synthetic analogue of dopamine that is administered intravenously in hospitals to reduce exacerbations of heart failure and to treat heart failure following cardiac surgery. It is not used often, as more established drugs like epinephrine, dopamine, dobutamine, norepinephrine, and levosimendan work as well. It works by stimulating beta-2 adrenergic receptors and peripheral dopamine receptor D1 and dopamine receptor D2. It also inhibits the neuronal re-uptake of norepinephrine.

<span class="mw-page-title-main">Adrenaline</span> Hormone and medication

Adrenaline, also known as epinephrine, is a hormone and medication which is involved in regulating visceral functions. It appears as a white microcrystalline granule. Adrenaline is normally produced by the adrenal glands and by a small number of neurons in the medulla oblongata. It plays an essential role in the fight-or-flight response by increasing blood flow to muscles, heart output by acting on the SA node, pupil dilation response, and blood sugar level. It does this by binding to alpha and beta receptors. It is found in many animals, including humans, and some single-celled organisms. It has also been isolated from the plant Scoparia dulcis found in Northern Vietnam.

Critical illness–related corticosteroid insufficiency is a form of adrenal insufficiency in critically ill patients who have blood corticosteroid levels which are inadequate for the severe stress response they experience. Combined with decreased glucocorticoid receptor sensitivity and tissue response to corticosteroids, this adrenal insufficiency constitutes a negative prognostic factor for intensive care patients.

<span class="mw-page-title-main">Norepinephrine (medication)</span> Therapeutic use of norepinephrine

Norepinephrine, also known as noradrenaline, is a medication used to treat people with very low blood pressure. It is the typical medication used in sepsis if low blood pressure does not improve following intravenous fluids. It is the same molecule as the hormone and neurotransmitter norepinephrine. It is given by slow injection into a vein.

<span class="mw-page-title-main">Dopamine (medication)</span> Hormone used as a medication

Dopamine, sold under the brandname Intropin among others, is a medication most commonly used in the treatment of very low blood pressure, a slow heart rate that is causing symptoms, and, if epinephrine is not available, cardiac arrest. In newborn babies it continues to be the preferred treatment for very low blood pressure. In children epinephrine or norepinephrine is generally preferred while in adults norepinephrine is generally preferred for very low blood pressure. It is given intravenously or intraosseously as a continuous infusion. Effects typically begin within five minutes. Doses are then increased to effect.

<span class="mw-page-title-main">Epinephrine (medication)</span> Hormone used as a medicine

Epinephrine, also known as adrenaline, is a medication and hormone. As a medication, it is used to treat several conditions, including anaphylaxis, cardiac arrest, asthma, and superficial bleeding. Inhaled epinephrine may be used to improve the symptoms of croup. It may also be used for asthma when other treatments are not effective. It is given intravenously, by injection into a muscle, by inhalation, or by injection just under the skin.

<span class="mw-page-title-main">Angiotensin II (medication)</span> Treatment for low blood pressure

Angiotensin II is a medication that is used to treat hypotension resulting from septic shock or other distributive shock. It is a synthetic vasoconstrictor peptide that is identical to human hormone angiotensin II and is marketed under the brand name Giapreza. The Food and Drug Administration approved the use of angiotensin II in December 2017 to treat low blood pressure resulting from septic shock.

Vasodilatory shock, vasogenic shock, or vasoplegic shock is a medical emergency belonging to shock along with cardiogenic shock, septic shock, allergen-induced shock and hypovolemic shock. When the blood vessels suddenly relax, it results in vasodilation. In vasodilatory shock, the blood vessels are too relaxed leading to extreme vasodilation and blood pressure drops and blood flow becomes very low. Without enough blood pressure, blood and oxygen will not be pushed to reach the body's organs. If vasodilatory shock lasts more than a few minutes, the lack of oxygen starts to damage the body's organs. Vasodilatory shock like other types of shock should be treated quickly, otherwise it can cause permanent organ damage or death as a result of multiple organ dysfunction.

References

  1. ↑ "Vasopressin Use During Pregnancy". Drugs.com. 22 January 2020. Retrieved 7 September 2020.
  2. ↑ "Diabetes Insipidus". National Institute of Diabetes and Digestive and Kidney Diseases. October 2015. Retrieved 28 May 2017.
  3. 1 2 3 "Pitressin (Injection)". Drugs.com. Retrieved 26 June 2017.
  4. 1 2 "Vasopressin (Injection Route)". mayoclinic.org. Retrieved 26 June 2017.
  5. ↑ "Competitive Generic Therapy Approvals". U.S. Food and Drug Administration (FDA). 29 June 2023. Archived from the original on 29 June 2023. Retrieved 29 June 2023.
  6. ↑ "Vasopressin" (PDF). F.A. Davis Company. 2017. Retrieved 2017-03-13.[ dead link ]
  7. ↑ Baum S, Nusbaum M, Tumen HJ (1970). "The control of gastrointestinal hemorrhage by selective mesenteric infusion of pitressin". Gastroenterology. 58: 926.
  8. ↑ Dünser MW, Mayr AJ, Ulmer H, Ritsch N, Knotzer H, Pajk W, et al. (July 2001). "The effects of vasopressin on systemic hemodynamics in catecholamine-resistant septic and postcardiotomy shock: a retrospective analysis". primary. Anesthesia and Analgesia. 93 (1): 7–13. doi: 10.1097/00000539-200107000-00003 . PMID   11429329. S2CID   41265162.
  9. ↑ Dünser MW, Mayr AJ, Tür A, Pajk W, Barbara F, Knotzer H, Ulmer H, Hasibeder WR (May 2003). "Ischemic skin lesions as a complication of continuous vasopressin infusion in catecholamine-resistant vasodilatory shock: incidence and risk factors". primary. Critical Care Medicine. 31 (5): 1394–8. doi:10.1097/01.CCM.0000059722.94182.79. PMID   12771608. S2CID   11514445.
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  18. 1 2 3 Williamson K, Breed M, Alibertis K, Brady WJ (February 2012). "The impact of the code drugs: cardioactive medications in cardiac arrest resuscitation". Emergency Medicine Clinics of North America. 30 (1): 65–75. doi:10.1016/j.emc.2011.09.008. PMID   22107975.
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  23. ↑ Gueugniaud PY, David JS, Chanzy E, Hubert H, Dubien PY, Mauriaucourt P, Bragança C, Billères X, Clotteau-Lambert MP, Fuster P, Thiercelin D, Debaty G, Ricard-Hibon A, Roux P, Espesson C, Querellou E, Ducros L, Ecollan P, Halbout L, Savary D, Guillaumée F, Maupoint R, Capelle P, Bracq C, Dreyfus P, Nouguier P, Gache A, Meurisse C, Boulanger B, Lae C, Metzger J, Raphael V, Beruben A, Wenzel V, Guinhouya C, Vilhelm C, Marret E (July 2008). "Vasopressin and epinephrine vs. epinephrine alone in cardiopulmonary resuscitation". The New England Journal of Medicine. 359 (1): 21–30. doi: 10.1056/NEJMoa0706873 . PMID   18596271.
  24. 1 2 Sillberg VA, Perry JJ, Stiell IG, Wells GA (December 2008). "Is the combination of vasopressin and epinephrine superior to repeated doses of epinephrine alone in the treatment of cardiac arrest-a systematic review". Resuscitation. 79 (3): 380–6. doi:10.1016/j.resuscitation.2008.07.020. PMID   18951676.
  25. ↑ Ong ME, Tiah L, Leong BS, Tan EC, Ong VY, Tan EA, Poh BY, Pek PP, Chen Y (August 2012). "A randomised, double-blind, multi-centre trial comparing vasopressin and adrenaline in patients with cardiac arrest presenting to or in the Emergency Department". Resuscitation. 83 (8): 953–60. doi:10.1016/j.resuscitation.2012.02.005. PMID   22353644.
  26. ↑ Mastropietro CW, Clark JA, Delius RE, Walters HL, Sarnaik AP (September 2008). "Arginine vasopressin to manage hypoxemic infants after stage I palliation of single ventricle lesions". Pediatric Critical Care Medicine. 9 (5): 506–10. doi:10.1097/pcc.0b013e3181849ce0. PMID   18679141. S2CID   30271090.
  27. 1 2 Mastropietro CW, Rossi NF, Clark JA, Chen H, Walters H, Delius R, Lieh-Lai M, Sarnaik AP (October 2010). "Relative deficiency of arginine vasopressin in children after cardiopulmonary bypass". Critical Care Medicine. 38 (10): 2052–8. doi:10.1097/ccm.0b013e3181eed91d. PMID   20683257. S2CID   46667831.
  28. 1 2 3 Mastropietro CW, Mahan M, Valentine KM, Clark JA, Hines PC, Walters HL, Delius RE, Sarnaik AP, Rossi NF (December 2012). "Copeptin as a marker of relative arginine vasopressin deficiency after pediatric cardiac surgery". Intensive Care Medicine. 38 (12): 2047–54. doi:10.1007/s00134-012-2731-9. PMID   23093248. S2CID   23426960.
  29. ↑ Mastropietro CW, Davalos MC, Seshadri S, Walters HL, Delius RE (June 2013). "Clinical response to arginine vasopressin therapy after paediatric cardiac surgery". Cardiology in the Young. 23 (3): 387–93. doi:10.1017/S1047951112000996. PMID   22805534. S2CID   26088566.
  30. ↑ Davalos MC, Barrett R, Seshadri S, Walters HL, Delius RE, Zidan M, Mastropietro CW (March 2013). "Hyponatremia during arginine vasopressin therapy in children following cardiac surgery". Pediatric Critical Care Medicine. 14 (3): 290–7. doi:10.1097/pcc.0b013e3182720473. PMID   23392370. S2CID   35061631.
  31. 1 2 3 Mastropietro CW, Miletic K, Chen H, Rossi NF (December 2014). "Effect of corticosteroids on arginine vasopressin after pediatric cardiac surgery". Journal of Critical Care. 29 (6): 982–6. doi:10.1016/j.jcrc.2014.07.007. PMID   25092616.
  32. ↑ Palm C, Pistrosch F, Herbrig K, Gross P (July 2006). "Vasopressin antagonists as aquaretic agents for the treatment of hyponatremia". The American Journal of Medicine. 119 (7 Suppl 1): S87–92. doi:10.1016/j.amjmed.2006.05.014. PMID   16843091.
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