In those early days-as a Pediatrician-I knew that the story of babies with hyaline
membrane disease, now called neonatal respiratory distress syndrome(RDS), was a sad
one. This disease was the most frequent cause of death of newborn babies, accounting
for hundreds of thousands of deaths annually worldwide. 1 also knew from Drs. Avery
and Mead's work in 1959 and a joint series of our earlier physiologic and biochemical
studies with professor Forrest H. Adams at UCLA on premature lambs and premature
infants over 15 years(1962-77) that the fundamental problem in RDS was the lack in the
lungs of these babies due to immaturity of a material known as "surfactant." Without
this material the newborn baby could not breath normally at birth, and the newborn
baby, must be provided with the surfactant as soon as possible, if there was to be any
chance for survival.
In 1962, 1 went to UCLA for a two-year sabbatical to study under Dr. Adams. Our
main joint effort over the next 15 years was on the general topic of fetal and neonatal
lung function. We quickly found that the lung fluid in fetal lambs contained surfactant,
and also that the fluid proceeded up the tracheobronchial tree carrying sufactant with it
into the amniotic cavity. In immature lambs there was no surfactant in either lung fluid
or amniotic fluid. These original findings led us to the idea that analysis of sufactant in
amniotic fluid might predict lung maturation. Dr. L. Gluck subsequently developed the
arrmiotic fluid US ratio, a predictor of neonatal respiratory disorss syndrome(RDS).
Subsequently, Dr. R. E. pattle, a discoverer of surfactant, cited our paper of
amniotic-fluid surfactant and developed a quick microbubble test for identifying babies
with surfactant deficiency at birth which now is widely used in the rest of NICUS of
the county.
It was natural that we asked ourselves "What is the lipid composition in the lungs of
infants with RDS?" So, we analyzed the lipid content in the lungs obtained at autopsy
from premature infants who had died in the immediate neonatal period. Although active
phospholipid components were present in the lungs of very small premature fetuses and
in the infants dying of RDS, the Quantity of active components was low6.
Thus, We confirmed the Avery and Mead's hypothesis that primary surfactant
deficiency probably was the cause of RDS.
After I returned to Sendai in June 1964, 1 set up my own laboratory and I found that
an organic solvent extract of calf lung surfactant(free of hydrophilic surfactant proteins)
was the only surface-active component of natural surfactant. Although this finding
received little attention at that time, it eventually led me to develop an effective artificial
surfactant for the treatment of RDS in the late 1970s.
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