Effects of inhaled nitric oxide and surfactant with extracorporeal life support in recovery phase of septic acute lung injury in piglets

Inhaled NO Contributes to Lung Repair in Piglets with Acute Respiratory Distress Syndrome via Increasing Circulating Endothelial Progenitor Cells

“…ARDS was defined as PaO 2 /FiO 2 ≤200 mmHg, with dynamic lung compliance (Cdyn) decreased by more than 50% from its baseline level, and histological evidence of bilateral infiltration of inflammatory cells in the lung (verified by our pilot study in 2 additional piglets) according to previous reports [25], [26]. The moment lung injury was established was defined as treatment time 0 h. There were no differences in the body weight among the four groups, and no difference in PaO 2 /FiO 2 and Cdyn was found among ARDS, iNO and G-CSF group at time 0 (Table 1, Table S1).…”

“…The animals were randomly assigned into each of the following 4 groups (n = 6 each): Con group, where normal animals were ventilated; ARDS group, which was established and treated with mechanical ventilation; G-CSF group, where a subcutaneous injection of G-CSF (a commonly used agent for EPCs mobilizing) was administered to ARDS animals at a dose of 10 µg/kg daily for 7 days; and iNO group, where inhaled NO (10 ppm) was administered to ARDS animals during ventilation and NO gas at 1000 ppm (Noventek) was supplied to the inspiratory line of the ventilator circuit [25]–[27].…”

“…Sections stained with hematoxylin and eosin were examined by light microscopy for injury patterns and severity as assessed by lung injury scores for edema, neutrophil infiltration, hemorrhage and bronchiole epithelial desquamation [25], [26], [30].…”

“…Recently, it has been reported that iNO restored vessel density and improved lung structure in neonatal rat model of bronchopulmonary dysplasia (BPD) [23]. Our previous animal studies also indicated that inhaled NO can attenuate the lung injury score in hyperoxic lung injury and ALI animals [24], [25]. However, it is unknown whether iNO can mobilize bone marrow EPCs and consequently promote lung vascular repair.…”

Mobilization of Endothelial Progenitor Cells From Bone Marrow is Impaired in a Piglet Model of Acute Respiratory Distress Syndrome*

“…ARDS was defined as Pao 2 /Fio 2 less than or equal to 200 mm Hg (26.6 kPa) and Cdyn decrease of more than 50% compared to baseline level (29). Oleic acid (Sigma, St. Louis, MO) was infused over 30 minutes via central venous catheter.…”