Arginine vasopressin (AVP) is a nine amino acid peptide hormone, which is synthesized in the hypothalamus as a precursor, transported down the portal system and stored in the posterior pituitary gland. It is also known as argipressin or antidiuretic hormone (ADH) and it is closely related in structure to oxytocin, which is also released from the posterior pituitary. Physiologically, it acts though the kidney with several other hormones to conserve solute-free water, but in hypovolemic states its potent arterial and venoconstrictor properties act to preserve blood pressure. Vasopressin has been used for many years in the treatment of diabetes insipidus and in control of bleeding esophageal varices (utilizing its potent vasoconstrictor effect on the slanchnic circulation), but its role as a pressor agent in the context of resuscitation, septic shock and pediatric cardiac surgery has only emerged in the last few years. Vasopressin is released physiologically in response to a rise in osmolarity, which is sensed within sensitive receptors in the hypothalamus. A fall in osmolarity below 280 mOsmAEkg will trigger its release (1). It acts via V2 receptors to open aquaporin (water channels) in the collecting tubules thereby increasing central water reabsorption. Reduction in afferent transmission from baroreceptors or cardiopulmonary volume receptors associated with hypovolemia or hypotension will also trigger vasopressin release which then acts via V1a receptors of smooth muscle to produce vasoconstriction of both veins and arteries (2). Similarly, increases in circulating ANG11 act via the hypothalamus to trigger release (3). The vasoconstictive effects are specific to different organ beds with the slanchnic bed being particularly sensitive to the circulating concentrations of vasopressin. In addition, increase in vasopressin activity is associated with increased release of corticotrophin releasing hormone via V1b (V3) receptors within the CNS, an increase in release of FV111, Von Willebrand Factor and enhanced platelet aggregation. The physiological effects on the heart are unclear. In the isolated healthy myocyte AVP produces improved contractility (4) probably by increasing intracellular calcium in myocardial cells through a GTP mechanism (5): The integrated position is less clear: pharmacological doses cause coronary vasoconstriction, while improved inotropic performance in pathological states may occur due both primary myocardial effect of secondary effects because of improved coronary perfusion. Pathologically, vasopressin is known to rise in heart failure and conditions of cardiovascular compromise. There are less data in children: in a study of neonates with congenital heart disease, AVP levels in infants with congestive heart and no outflow tract obstruction was significantly higher than normal controls but those with failure and left ventricular outflow tract obstruction had reduced levels (6). The available data suggest that while vasopressin levels are often raised appropriately in hypotensive states because of a variety of conditions this is not necessarily the case. Small studies have been published documenting vasopressin deficiency in catecholamine resistant hypotension (7,8). Vasopressin became of interest when it was observed that organ donors who had brain death and diabetes insipidus were cardiovascularly more stable with reduced inotrope requirements and better organ preservation. Additionally, it was observed that patients who survived cardiac arrest had higher levels of vasopressin compared to nonsurvivors (9). In contrast, there is a correlation of poorer outcome after cardiopulmonary resuscitation with higher levels of endogenous catecholamines (10). These observations led to initial adult studies which questioned whether the purer vasoPediatric Anesthesia 2008 18: 579–581 doi:10.1111/j.1460-9592.2008.02520.x
Read full abstract
Mar 29, 2018
G R Vagapova 
Open Access
