When does prone sleeping improve cardiorespiratory status in preterm infants in the NICU?

STUDY OBJECTIVES: Preterm infants undergoing intensive care are often placed prone to improve respiratory function. Current clinical guidelines recommend preterm infants are slept supine from 32 weeks' postmenstrual age, regardless of gestational age at birth. However, respiratory function is also related to gestational and chronological ages and is affected by sleep state. We aimed to identify the optimal timing for adopting the supine sleeping position in preterm infants, using a longitudinal design assessing the effects of sleep position and state on cardiorespiratory stability. METHODS: Twenty-three extremely (24-28 weeks' gestation) and 33 very preterm (29-34 weeks' gestation) infants were studied weekly from birth until discharge, in both prone and supine positions, in quiet and active sleep determined by behavioral scoring. Bradycardia (heart rate ≤100 bpm), desaturation (oxygen saturation ≤80%), and apnea (pause in respiratory rate ≥10 s) episodes were analyzed. RESULTS: Prone positioning in extremely preterm infants reduced the frequency of bradycardias and desaturations and duration of desaturations. In very preterm infants, prone positioning only reduced the frequency of desaturations. The position-related effects were not related to postmenstrual age. Quiet sleep in both preterm groups was associated with fewer bradycardias and desaturations, and also reduced durations of bradycardia and desaturations in the very preterm group. CONCLUSIONS: Cardiorespiratory stability is improved by the prone sleep position, predominantly in extremely preterm infants, and the improvements are not dependent on postmenstrual age. In very preterm infants, quiet sleep has a more marked effect than the prone position. This evidence should be considered in individualizing management of preterm infant positioning.

Effects of Prone Sleeping on Cerebral Oxygenation in Preterm Infants.

OBJECTIVE: To determine the effect of prone sleeping on cerebral oxygenation in preterm infants in the neonatal intensive care unit. STUDY DESIGN: Preterm infants, divided into extremely preterm (gestational age 24-28 weeks; n = 23) and very preterm (gestational age 29-34 weeks; n = 33) groups, were studied weekly until discharge in prone and supine positions during active and quiet sleep. Cerebral tissue oxygenation index (TOI) and arterial oxygen saturation (SaO2) were recorded. Cerebral fractional tissue extraction (CFOE) was calculated as CFOE = (SaO2 - TOI)/SaO2. RESULTS: In extremely preterm infants, CFOE increased modestly in the prone position in both sleep states at age 1 week, in no change in TOI despite higher SaO2. In contrast, the very preterm infants did not have position-related differences in CFOE until the fifth week of life. In the very preterm infants, TOI decreased and CFOE increased with active sleep compared with quiet sleep and with increasing postnatal age. CONCLUSION: At 1 week of age, prone sleeping increased CFOE in extremely preterm infants, suggesting reduced cerebral blood flow. Our findings reveal important physiological insights in clinically stable preterm infants. Further studies are needed to verify our findings in unstable preterm infants regarding the potential risk of cerebral injury in the prone sleeping position in early postnatal life.

Escherichia coli abg genes enable uptake and cleavage of the folate catabolite p-aminobenzoyl-glutamate.

Escherichia coli AbgT was first identified as a structural protein enabling the growth of p-aminobenzoate auxotrophs on exogenous p-aminobenzoyl-glutamate (M. J. Hussein, J. M. Green, and B. P. Nichols, J. Bacteriol. 180:6260-6268, 1998). The abg region includes abgA, abgB, abgT, and ogt; these genes may be regulated by AbgR, a divergently transcribed LysR-type protein. Wild-type cells transformed with a high-copy-number plasmid encoding abgT demonstrate saturable uptake of p-aminobenzoyl-glutamate (K(T)=123 microM); control cells expressing vector demonstrate negligible uptake. The addition of metabolic poisons inhibited uptake of p-aminobenzoyl-glutamate, consistent with this process requiring energy. p-Aminobenzoyl-glutamate taken in by cells expressing large amounts of AbgT alone is not rapidly metabolized to a form that is trapped in the cell, as the addition of nonradioactive p-aminobenzoyl-glutamate to these cells results in a rapid loss of intracellular label. The addition of nonradioactive p-aminobenzoate has no effect. The abgA, abgB, and abgAB genes were cloned into the medium-copy-number plasmid pACYC184; p-aminobenzoate auxotrophs transformed with the clone encoding abgAB demonstrated enhanced ability to grow on low levels of p-aminobenzoyl-glutamate. When transformed with complementary plasmids encoding high-copy levels of abgT and medium-copy levels of abgAB, p-aminobenzoate auxotrophs grew on 50 nM p-aminobenzoyl-glutamate. Our data are consistent with a model of p-aminobenzoyl-glutamate utilization in which AbgT catalyzes transport of p-aminobenzoyl-glutamate, followed by cleavage to p-aminobenzoate by a protein composed of subunits encoded by abgA and abgB. While endogenous expression of these genes is very low under the conditions in which we performed our experiments, these genes may be induced by AbgR bound to an unknown molecule. The true physiological role of this region may be related to some molecule similar to p-aminobenzoyl-glutamate, such as a dipeptide.