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Changes in the spatial distribution of pulmonary blood flow during the fetal/neonatal transition: an in vivo study in the rabbit
Author(s) -
Lipsett Jill,
Hunt Kerri,
Carati Colin,
Gan Bren
Publication year - 1989
Publication title -
pediatric pulmonology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.866
H-Index - 106
eISSN - 1099-0496
pISSN - 8755-6863
DOI - 10.1002/ppul.1950060402
Subject(s) - fetus , lung , medicine , blood flow , fetal circulation , perfusion , in vivo , pathology , cardiology , biology , pregnancy , genetics , microbiology and biotechnology , placenta
The spatial distribution of pulmonary blood flow was investigated in term fetal and neonatal rabbit littermates, using the plasma tracer fluorescein‐isothiocyanate bovine serum albumin (FITC‐BSA). A tracer bolus was injected intravenously and allowed 2 minutes to circulate in vivo, prior to arrest of the circulation and tissue preparation. In the fetus, fluorescence was only present in 43% of the lung volume, contained within discrete regions or “lobules.” Some 57% of lung volume received no tracer inflow at all (during 2 min). In the fetal lung, the size of the potential airspaces in the perfused regions was 1.5 times larger than those in the nonperfused regions. In the fetus, a high pulmonary vascular resistance (PVR) is maintained. It is generally accepted that pulmonary blood flow in the fetus is evenly distributed to the entire vascular bed. Our results show that fetal pulmonary blood flow is distributed to discrete “lobules,” while (over a 2 min period) the majority of “lobules” receive no flow at all. Thus, by directing flow to a lesser proportion of the vasculature, greater flow rates are achieved, and the risk of blood sludging and stasis is reduced. Alternation of perfusion with nonperfusion in each “lobule,” perhaps regulated by the lobular arterioles, would permit both maintenance of the high fetal PVR and uniform lung development. In the neonatal lung, the plasma tracer was distributed uniformly to the entire vascular bed. This suggests that some of the reduction in PVR at birth is due to recruiting 50–60% of lung vasculature.