Am. J. Respir. Crit. Care Med., Vol 151, No. 6, Jun 1995, 1989-1997.
Surfactant protein-A deficiency in a primate model of bronchopulmonary dysplasia
RJ King, JJ Coalson, RA deLemos, DR Gerstmann and SR Seidner
Department of Physiology, University of Texas Health Science Center at San Antonio 78284-7756, USA.
Pathophysiologic and biochemical (surfactant protein and phospholipid)
features were studied in a baboon model of hyperoxia-induced
bronchopulmonary dysplasia (BPD) and superimposed infection. A total of 20
baboons were delivered by hysterotomy at 76% of gestation (140 d of
gestational age) and were randomized into four groups, consisting of two
control and two injury groups. Animals constituting a group that was
managed on a pro re nata (PRN) basis were ventilated with clinically
appropriate oxygen for the 16-d experimental period and served as
ventilatory controls. They underwent an initial period of 42 h during which
they demonstrated evidence of hyaline membrane disease (HMD), but began
recovery at 42 h and by Day 6 appeared to have maximally recovered. At the
time of these animals' killing, concentrations of surfactant proteins,
messenger ribonucleic acids (mRNAs), and phospholipids were similar to
those of normal adult baboons. Gestational control animals were delivered
and killed without ventilation at 156 d gestational age. Surfactant
protein-A (SP-A) and phospholipid concentrations in these animals' lavage
fluids were about 10% of those in the PRN animals. Animals with BPD were
subjected to positive-pressure ventilation and an FIO2 of 1.0 for 11 d,
followed by 5 d of an FIO2 sufficient to maintain PaO2 at 40 to 50 mm Hg.
The animals with BPD and infection were treated in the same way as the BPD
group, except that 10(8) Escherichia coli were instilled intratracheally on
Day 11, concomitantly with the reduction in FIO2.(ABSTRACT TRUNCATED AT 250
WORDS)
