الفهرس 
PHYSIOLOGICALANDPHARMACOLOGICALASPECTS OFVASOPRESSINOnly 14 pages are availabe for public view
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Abstract
V
asopressin is synthesized by magnocellular neurons of the hypothalamus and stored in the posterior lobe of the pituitary gland. Vasopressin is involved in the maintenance of blood osmolarity and volume, by its effects on the kidneys, and in the control of blood pressure, by its constrictor effects on vascular smooth muscles.
Vasopressin binds to different types of receptors to perform its action. The V1 receptors located in vascular smooth muscles, platelets, and hepatocytes causing vasoconstriction. The V2 receptors located in the kidneys facilitating the urine concentrating mechanism. The V3 receptors by activation of adrenocorticotropin hormone (ACTH) secretion in the pituitary. It binds also to oxytocin and purinergic receptors.
Inotropes are agents administered to increase myocardial contractility whereas vasopressor agents are administered to increase vascular tone. The use of these potent agents is largely confined to critically ill patients with profound haemodynamic impairment such that tissue blood flow is not sufficient to meet metabolic requirements.
Most of vasopressors and inotropes act on adrenergic receptors and some act on dopaminergic receptors and some act by inhibiting phosphodiesterase receptors.
Shock is an acute or hyperacute physiological derangement, a systemic syndrome characterized by signs and symptoms, which are the response of different organs to a situation of hypoperfusion for their cells basic metabolic needs. There are practically four categories of shock: Cardiogenic, hypovolemic and inflammatory, which can be subdivided in septic and toxic shock.
It was found that infusion of 0.04 U/min of vasopressin improve patients with hypovolemic shock especially in hemorrhagic states. By understood mechanisms vasopressin can influence secretion of potassium in the distal nephron.
Infusion of an “ultra-low” dose vasopressin (0.03 U/min) during cardiopulmonary bypass and for the first four hours after coronary artery bypass grafting in patients having low ejection fraction, is safe and beneficial. It significantly reduces the required doses of catecholamines, obtaining a better hemodynamic profile, a higher urine output, lower blood loss for the first 24 hours and prevention from the incidence of post-cardiotomy vasodilatory shock.
According to The Surviving Sepsis Campaign Guidelines for Management of Severe Sepsis and Septic Shock vasopressin 0.03 units/minute can be added to norepinephrine with intent of either raising mean arterial blood pressure or decreasing norepinephrine dosage.
Vasopressin infusion in septic shock increases blood pressure, decreases requirements for norepinephrine and improves renal function. Vasopressin plus corticosteroid treatment may decrease mortality compared to corticosteroids plus norepinephrine. Potential mechanisms are that vasopressin plus corticosteroids beneficially alter immunity in septic shock.
The American Heart Association released revised guidelines for cardiopulmonary resuscitation. The consensus was that, vasopressors should be given during cardiac arrest with 1 mg dose of IV/IO epinephrine every 3 to 5 minutes. The guidelines also recommend that vasopressin (40 units IV) can replace the first or second dose of epinephrine.
In out-of-hospital cardiac arrests, vasopressin was found to be comparable to epinephrine when the rhythm was ventricular fibrillation or pulseless electrical activity but superior to epinephrine for patients in asystole. Vasopressin is superior to epinephrine for increasing vital organ blood flow, in particular coronary and cerebral blood flow, when administered intravenously as well as endobronchially or via the intraosseous route.