**1. Introduction**

Involving more commonly the premature (less than 37 weeks of gestational age) infants, neonatal respiratory distress syndrome (NRDS), is an important clinical syndrome responsible for a high rate of mortality and morbidity. Reports have shown that about 12% of infants are preterm in the United States, while the prevalence ranges between 6 and 11% in European countries [1, 2]. NRDS is a leading cause of admission to neonatal intensive care unit (NICU) with estimated incidence rate of 7.8% and mortality rate of 50% in premature infants [3–5]. The severity usually increases during the first 48 hours of birth [6]. The prevalence and the severity of NRDS decrease as the gestational age increases [7–9].

A variety of factors including cesarean section, prematurity, maternal diabetes and genetic variations have been reported to play role in pathogenesis of NRDS [10, 11]. Damage to type II alveolar cells is another considered mechanism for NRDS. Diffuse alveolar capillary injury results in progressive increased permeability as well as pulmonary and alveolar edema, which make the type II alveolar cells nonfunctional. All these processes lead into severe hypoxemia due to abnormal ventilation/perfusion ratio [12, 13].

NRDS is a result of pulmonary immaturity mostly caused by insufficient levels of surfactant [14, 15]. The condition is developed through hypoventilation, hypoxemia and respiratory acidosis [14, 15].
