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This Article Full Text Full Text (PDF) All Versions of this Article: 288/3/L562    most recent 00220.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Benachi, A. Articles by Bourbon, J. R. Search for Related Content PubMed PubMed Citation Articles by Benachi, A. Articles by Bourbon, J. R.

Surfactant phospholipids and proteins are increased in fetal sheep with pulmonary hypertension secondary to fetal systemic arteriovenous fistula

¹Institut National de la Santé et de la Recherche Médicale U492, Faculté de Médecine, Créteil; ²Maternité, Hôpital Necker-Enfants Malades, Assistance Publique-Hôpitaux de Paris-Université Paris V; and ³Service de Gynécologie-Obstétrique, Hôpital Rothschild, Assistance Publique-Hôpitaux de Paris-Université Paris VI, Paris, France

Submitted 11 June 2004 ; accepted in final form 17 November 2004

To determine whether prenatal surfactant storage was altered in a model of systemic arteriovenous fistula (SAVF) with pulmonary hypertension, a fistula was created between the internal jugular vein and the carotid artery in 120-day fetal lambs, and surfactant material was explored at 134 days. Total phospholipids (TPL) and disaturated phosphatidylcholine (DSPC) were increased in whole lung tissue. Phospholipid analysis of isolated lamellar body fraction evidenced a specific increase of surfactant pool size: TPL and DSPC in this fraction were enhanced 1.9 and 2.9 times, respectively, when referred to DNA. Although the steady-state level of transcripts of surfactant protein (SP)-A and SP-B was not found to be changed at the time of death, semiquantitative Western blot analysis revealed elevated SP-A and SP-B protein contents three- and twofold, respectively. These findings indicate markedly enhanced accumulation of surfactant material in the presence of surgically induced prenatal pulmonary hypertension. Although total lung cell number was increased by 26%, SP-B immunolabeling indicated that increased surfactant amount did not result from an increased alveolar type II cell proportion, but rather from an increased rate of storage. Whether similar changes in surfactant are encountered in human neonates with persistent pulmonary hypertension is worthy of investigation.

fetus; lung surfactant; alveolar type II cells; disaturated phosphatidylcholine