Influence of upper respiratory tract on liquid flow to and from fetal lungs

Abstract

The experiments were designed to determine the influence of the upper respiratory tract (URT) on liquid flow in the fetal trachea. This flow probably influences pulmonary distension, which is thought to be a major determinant of prenatal lung development. In six fetal sheep the URT could be bypassed by connecting the lower trachea, via an external flowmeter, to a cannula in the amniotic sac. In confirmation of our earlier findings, when the URT was in circuit, the mean rate of tracheal efflux was greater during episodes of fetal breathing movements (FBM) [mean 13.8 +/- 2.6 (SE) ml/h] than during apneic periods (mean 3.2 +/- 1.0 ml/h). When the URT was bypassed there was a reversal of net tracheal flow during FBM episodes (mean 19.6 +/- 5.6 ml/h toward the lungs); during apnea there was a much greater rate of efflux (mean 33.1 +/- 10.2 ml/h) than when the URT was in circuit. Nonlabor uterine contractions were associated with an increased rate of efflux during apnea only when the URT was bypassed. We conclude that during fetal life the URT imposes an essentially unidirectional flow of pulmonary liquid away from the lungs, preventing ingress of amniotic fluid and maintaining constancy of composition of liquid in the developing airways. By retarding outward flow during periods of apnea and thoracic compression and by preventing net influx during episodes of FBM, the URT has the probable effect of maintaining the volume and composition of liquid in the fetal airways within narrow limits.

Lung Hypoplasia Can Be Reversed by Short-Term Obstruction of the Trachea in Fetal Sheep

“…In contr ast, after tracheal obstruction lung liquid volumes progressively increased to control values after 6 d, and associated with this increase in volume was an increase in tracheal pressure; the values measured were similar to the values we recorded in fetuses exposed to 7 d of tracheal occlusion (4). Consequently, we sugges t that the generation of an intraluminal pressur e that will expand the hypoplastic fetal lung to a level that will significantly stimulate lung growth, must be dependent upon the presence of a resistance to lung liquid efflux that is greater than that which norm ally occurs during fetal apnea as a result of glottic narrowing (15,16). Indeed, the mean tracheal pressure measured in one fetus after reconnection of the tracheal circuit (drain and reconnect, 3.4 ± 0.4 mm Hg) was simil ar to that measured in control fetuses at the same age.…”

“…Furthermore, we sugges t that the failure of the hypoplastic lung to expand, in the absence of tracheal obstruction, is most probably the consequence of a relatively incompli ant lung and, perhaps more importantly, chest wall (23). Under these conditions, the normal resistance to lung liquid efflux offered by the upper airway (15,16) is prob ably insufficient to promote fluid accumulation and, therefore, increase lung expansion to the level required to stimulate lung grow th. In contrast, obstruction of the trachea in fetu ses with hypopl astic lung s quickl y increases the degree of lung expansion to normal levels, accelerat es lung growth and rever ses the lung growth deficit in as little as 6 d. Our findin gs support the recent observati ons that occlusion of the trach ea increases lung growth in fetal sheep with hypopl astic lung s indu ced by either herniation of the fetal diaph ragm (24) or nephrectomy (5) .…”

Sudden Infant Death Syndrome and Sudden Intrauterine Unexplained Death: Correlation Between Hypoplasia of Raphé Nuclei and Serotonin Transporter Gene Promoter Polymorphism

“…Since the correlation of L allele with raphé nuclei hypoplasia was found in our study also in high percentage of SIUD, it is reasonable to speculate whether breathing alterations can lead to death during intrauterine life. We know that periodic fetal breathing regulates the release of tracheal fluid in the lung, and consequently alveolar expansion, to favor lung development (33,34). Nevertheless, defective intrauterine respiratory movements would not be sufficient to justify fetal loss.…”

The Changing Landscape in Supporting Preterm Infants at Birth

“…The larynx is adducted in the fetus to restrain the efflux of lung fluid and to promote lung expansion and lung growth, while after birth, larynx abduction is required to enable lung aeration [8, 17, 18]. However, there is evidence that the larynx continues to function as during fetal life, remaining mostly closed during apnea and only opening briefly when a breath is taken.…”