الفهرس | Only 14 pages are availabe for public view |
Abstract SUMMERY RDS is one of the commonest causes of morbidity in pre term infants. It is caused by deficiency of surfactant, a lipoprotein responsible in lowering the surface tension in. the alveoli, which results in decrease lung compliance, and alveolar hypoventilation (Martin and Fanaroff, 1997). The cost of NICU due to RDS, mechanical ventilation and length of hospital stay is increasing with increased prematurity and severity of RDS (Gilbert et aI., 2003). Carnitine (L-3-hydroxy-4-N-trimethylaminobutyrate) IS a small, water soluble molecule that plays a key role in transporting long chain fatty acids across the barrier of the inner mitochondrial membrane for j3 - oxidation via a Carnitine acyltransferase enzyme system (Scaglia and Longo,. 1999). Enhanced transplacental transfer of Carnitine in earlier stages of pregnancy is thought to result in higher plasma Carnitine levels in preterm infants (Giannacopoulou et al.,1998). In contrast, tissue carnitine levels are directly proportional to the advancing gestational age and thus, preterm infants have lower tissue Carnitine reserves (Shenai and Borum, 1984). Pulmonary surfactant production is an important process in fetal lung maturation. As Carnitine is an integral component of the membrane phospholipid fatty acid turnover in human cells, it is possible that Carnitine causes lung maturation via membrane phospholipid repair activity (Arenas et al., 1998). Our aim was to investigate the status of free Carnitine level in maternal and neonatal plasma of preterm infants with respiratory distress syndrome (R.D.S) in the first hours of life. |