The Role of Arginine-Vasopressin in the Regulation of Water Metabolism in Preterm Infants in the First Days of Life

Abstract

We studied the role of arginine-vasopressin (AVP) in the regulation of fluid homeostasis in preterm infants. Group 1 was fed orally, groups 2 and 3 received fluids parenterally, and group 3 developed respiratory distress syndrome (RDS) and had to be ventilated. The infants of group 3 were not able to excrete the administered fluid, gained weight and consecutively developed hyponatremia. 1 -min Apgar scores as well as log FiO₂ correlated significantly with urinary AVP excretion on day 1. We conclude that nonosmotic stimuli are involved in the release of AVP and therefore disturb fluid homeostasis in severely ill infants with RDS.

A Comparison of Arginine Vasopressin Levels and Fluid Balance in the Perinatal Period in Infants Who Did and Did Not Develop Chronic Oxygen Dependency

“…Increased urinary [15] and plasma [14,16,17] AVP levels have been reported in infants with respiratory distress syndrome (RDS). In one series [17], comparison of results from three groups of preterm infants demonstrated that those with RDS were unable to excrete the administered fluid, gained weight and developed hyponatraemia.…”

“…In one series [17], comparison of results from three groups of preterm infants demonstrated that those with RDS were unable to excrete the administered fluid, gained weight and developed hyponatraemia. In animal models positive pressure ventilation is also a stimulus for AVP release [18], but the effect of ventilation on AVP levels in the human is debated [3,11,[19][20][21].…”

Monoclonal Antibodies

“…However, glomerular immaturity blunts the postnatal increase in glomerular filtration rate (Aperia et al, 1981) and so decreases the efficiency of ANP-induced water excretion. Over-hydration increases the risk that premature infants will develop patent ductus arteriosus, congestive heart failure (Bell et al, 1980), respiratory distress syndrome (Stegner et al, 1987) and bronchopulmonary dysplasia (Brown et al, 1978).…”

“…Infants with respiratory distress syndrome usually receive positive-pressure ventilation. The increased thoracic pressure causes decreased venous return to the heart and so stimulates the baroreceptors to promote AVP secretion (Rees et al, 1984a;Wiriyathian et al, 1986;Stegner et al, 1987) that correlates with the ventilation pressure (Stegner et al, 1987) and may cause water retention (Bell and Oh, 1979;Stegner et al, 1987). However, tubular function develops later than glomerular function so premature infants have a lower capacity than full-term infants to carry out AVP-induced water reabsorption (Aperia et al, 1981).…”

“…Inappropriate AVP secretion is common in premature infants, occurring in response to non-osmotic stimuli such as birth asphyxia (Wiriyathian et al, 1986;, respiratory distress, pneumothorax, intracranial haemorrhage (Rees et al, 1984a;Wiriyathian et al, 1986;Sulyok, 1988) or meningitis (Rees et al, 1980;Sulyok, 1988). The highest AVP concentrations occur in the most severely ill infants (Stegner et al, 1987;, who are therefore least able to excrete a water load. Birth asphyxia causes particularly high AVP concentrations (Wiriyathian et al, 1986;) but may be complicated by tubular damage that decreases the urine concentrating capacity (Svenningsen and Aronson, 1974;Aperia et al, 1983) or by glomerular damage which decreases urine output .…”