Abstract
In addition to its antidiuretic properties, arginine vasopressin (AVP) is a potent vasoactive homone. If unopposed by baroreceptor mediated reflexes, even low serun levels of AVP nay exert pressor effects. Since early life is associated with an enhanced ability to release AVP and with an increase in its cardiovascular effects, we evaluated whether congestive heart failure (CHF) is a stimulus for AVP release. AVP levels were measured by RIA using the modified Bentonite technique in 40 infants and children divided into 5 groups: Group I (n = 7) with CHF; Group II (n = 6) with cyanotic heart disease; Group III(n = 3) with persistent neonatal pulmonary hypertension; Group IV (n = 12) stressed infants with respiratory disease but no heart disease; and Group V (n = 12) healthy unstressed controls. Group IV had statistically higher AVP levels (13 pcg/ml ± 6) when compared to Group V normals (6 peg/ml ± 2)(p ≤ 0.05). Groups II & III were not significantly different from Group V (7 pcg/ml ± 5 and 6 peg/ml ± 2 respectively). CHF patients (Group I) had variable AVP levels with peak levels markedly elevated above other groups (102 peg/ml ± 135), (p<0.05) and further increased with worsening clinical status. Additional data suggest that hyperosrrotic angiographic contrast madia increase AVP levels by 2 to 10 times pre-dye levels in most instances (n = 12 of 15 patients, p < 0.02). We conclude that AVP levels are increased in children with CHF and that diagnostic interventions such as angiography may further elevate AVP. This may result in increased cardiac afterload further impairing already diminished cardiac function.
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