Published ahead of print on October 22, 2004, doi:10.1164/rccm.200406-774OC
Am. J. Respir. Crit. Care Med., Volume 171, Number 5, March 2005, 488-493
A more recent version of this article appeared on March 1, 2005
Submitted on June 18, 2004
Accepted on October 19, 2004
Surfactant and Physiological Responses of Preterm Lambs to Continuous Positive Airway Pressure
Neil Mulrooney1, Zahra Champion2, Timothy J.M. Moss3, Ilias Nitsos3, Machiko Ikegami1, and Alan H Jobe1*
1 Division of Pulmonary Biology, Cincinnati Children's Hospital, University of Cincinnati School of Medicine, Cincinnati, OH, United States,
2 Fisher and Paykel Healthcare, Ltd., Auckland, New Zealand,
3 University of Western Australia, School of Women's and Infants' Health, Perth, Australia
* To whom correspondence should be addressed. E-mail: alan.jobe{at}chmcc.org.
Although continuous positive airway pressure (CPAP) is used frequently for preterm infants, the relationships between the amount of surfactant and lung physiologic and injury responses to CPAP are unknown. Therefore, saturated phosphatidylcholine (Sat PC) was measured to quantify the surfactant necessary for preterm lambs to breathe successfully on a CPAP of 5 cm H2O (CPAP 5). 5 of 21 lambs delivered at 130-136 days gestation failed to keep Pco2 below 100 mmHg by 2 hours. The lambs that failed had < 1.9 mmol/kg Sat PC in BALF (about 3% the pool size at term), less surfactant secretion and less large aggregate surfactant. Physiologic responses of other 132 day preterm lambs after 2 or 6 hours of CPAP 5, CPAP 8 or mechanical ventilation then were characterized. At 6 hours, oxygenation and lung gas volumes were higher with CPAP 8 relative to the other groups and minute ventilation was decreased with CPAP 8 relative to CPAP 5. Lung dry/wet ratios were greater for the CPAP groups than for the mechanical ventilation group. A small amount of endogenous Sat PC is required for preterm lambs to breathe successfully with CPAP. CPAP 8 improves early newborn respiratory transition relative to CPAP 5.
Key words: respiratory distress syndrome, lung injury, cytokines, phosphatidylcholine
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