Professor Pillow and her team discovered that the preterm diaphragm is weaker than the diaphragm of babies born after a normal and complete gestation. This may be due to increased breakdown of the muscle protein and increased susceptibility to damage from oxygen free radicals.
Respiratory disease is the leading cause of death in preterm babies. Professor Jane Pillow and her team explored the factors hindering development of the diaphragm. They discovered that infection during pregnancy and maternal steroid treatment weakened the diaphragm, contributing to breathing difficulties after birth. These discoveries have opened a new area of focus in improving respiratory outcomes for preterm babies.
The diaphragm is the major muscle involved in breathing and normal functioning of the diaphragm is essential to survival. Professor Pillow’s research strives to understand how the diaphragm develops and how impaired diaphragm function contributes to breathing difficulties after birth in preterm babies.
The team studied diaphragms of preterm lambs to determine if exposure to common events such as maternal steroids or infection of the womb affects diaphragm development in an unborn baby.
Through this research, Professor Pillow and her team discovered that the preterm diaphragm is weaker than the diaphragm of babies born after a normal and complete gestation. This may be due to increased breakdown of the muscle protein and increased susceptibility to damage from oxygen free radicals.
Professor Pillow explained that the diaphragm is further impaired when the fetus is exposed to infection in the womb or maternal steroids.
‘Preterm babies may be exposed to infection and other agents that interfere with diaphragm development, making breathing efforts weaker after birth and potentially leading to respiratory failure,’ she said.
‘Exposure to maternal steroids, which are often used to improve the lung development of foetuses that are likely to be born preterm, also appears to be harmful to diaphragm function.’
‘This research will provide a new opportunity to protect the preterm infant from developing chronic respiratory disease.’
Professor Pillow’s studies suggest that the timing of this exposure is critical; exposure early in gestation results in weaker diaphragms than those exposed closer to term gestation.
‘We were able to show that this weakness in the diaphragm could be partly reduced by preventing the inflammatory response through blocking a key component in the pathway called interleukin,’ she said.
These findings have the potential to benefit preterm babies at risk of acute and chronic respiratory disease.
‘As the diaphragm is the main muscle driving our ability to breathe independently; impaired diaphragm function decreases our ability to breathe without mechanical assistance,’ Professor Pillow explained.
‘Preventing diaphragm dysfunction through ventilatory or pharmacological treatments is likely to provide a new opportunity to protect the preterm infant from developing chronic respiratory disease.'
‘These findings will be of interest to clinicians and nurses treating preterm infants, and to the parents of the infants at risk for this disorder.'
