首页|Nitric oxide releasing nanoparticles reduce inflammation in a small animal model of ARDS
Nitric oxide releasing nanoparticles reduce inflammation in a small animal model of ARDS
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NSTL
Acute respiratory distress syndrome (ARDS) is a condition hallmarked by high permeability pulmonary edema and hypoxemic respiratory failure and is associated with high mortality. Current treatment protocols rely on improving O2 delivery, decreasing O2 consumption, and treating the underlying cause of the initial insult. In this study, we used a small rodent model of ARDS, where we induced lung injury with inhalation of lipopolysac-charide (LPS). We investigated three different treatments, namely inhaled NO at 70 ppm, inhaled NO at 140 ppm, and NO-np (10 mg/mL), compared with untreated rodents 72 h after initial insult. Concurrent with treatment, the fraction of inspired O2 was increased after 30 min from 21% to 40% and finally to 60%. At an FiO_2 of 60% and 72 h post induction of ARDS, NO-np treated mice had an arterial PO_2 (PaO_2) of 142 ± 9 mmHg, higher than mice treated with inhaled NO at 70 ppm (87 ± 5 mmHg, p = 8.4 x 10~-8) and inhaled NO at 140 ppm (107 ± 6 mmHg, p = 6.1 x 10~-6). Neutrophils in both the periphery (1.6 x 10~5 ± 0.4 x 10~5 cells) and bronchoalveolar lavage fluid (BALF; 2.7 x 10~5 ± 0.8 x 10~5 cells) were reduced in NO-np treated mice compared to mice treated with inhaled NO at 70 ppm (p = 0.0097, 2.4 x 10~5 ± 0.5 x 10~5 cells for periphery, p = 0.0075, 3.8 x 10~5 ± 0.8 x 10~5 cells for BALF). In summary, we found that treatment with NO-np improved arterial PO_2 at a high FiO_2 compared to inhaled NO alone and NO-np reduced both circulating and pulmonary interstitial neutrophil count, while inhaled NO did not. Future studies should aim to elucidate the precise mechanisms behind how NO-np mediate neutrophilic inflammation in ARDS.
NSTL
