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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.