Am J Perinatol 1995; 12(4): 235-239
DOI: 10.1055/s-2007-994461
ORIGINAL ARTICLE

© 1995 by Thieme Medical Publishers, Inc.

Hemodynamic Control of Atrial Natriuretic Peptide Plasma Levels in Neonatal Respiratory Distress Syndrome

Pekka Kääpä, Marko Seppänen, Pentti Kero, Henrik Ekblad, Olli Arjamaa, Olli Vuolteenaho
  • Department of Pediatrics, University of Turku, Turku, and Department of Physiology, University of Oulu, Oulu, Finland
Further Information

Publication History

Publication Date:
04 March 2008 (online)

ABSTRACT

To evaluate the contribution of the pulmonary and ductal hemodynamics on the cardiac atrial natriuretic peptide (ANP) synthesis and release in neonatal respiratory distress syndrome, serial blood samples for plasma C-terminal end, and the more stable N-terminal end (NT-proANP) of the propeptide were obtained. Simultaneous evaluation of the systolic pulmonary artery pressure (PAP) and magnitude of ductal shunting by the Doppler method were made of 37 distressed infants during the first 4 days of life. Both plasma ANP and NT-proANP rose after birth, peaked at 48 hours of age, and correlated significantly (r = 0.66; p < 0.001; n = 78) with each other. The initially high systolic PAP and, since the systemic arterial pressure (SAP) did not change, the PAP/SAP ratio declined slowly during the study period, as did the magnitude of ductal left-to-right shunting after an initial increase during the first hours after birth. Plasma NT-proANP had a positive correlation to the magnitude of ductal left-to-right shunting both during the first 2 and 4 days of life, but did not correlate with PAP, SAP, or PAP/SAP ratio during the same time periods. Eight infants with delayed closure of the ductus maintained elevated plasma NT-proANP values after the second day of life. Our data thus suggest that in neonatal respiratory distress syndrome the high plasma ANP levels are due to increased cardiac ANP synthesis and release and that the main determinant accounting for this high ANP production during the acute phase of the disease is persistent ductal left-to-right shunting with left atrial stretch rather than the high right cardiac afterload.