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High School Student with a Traditionally Underrepresented Background

HS Poster

Poster 146 - Surfactant Replacement Therapy in a Rodent Model of Acute Respiratory Distress Syndrome

Saturday, October 26, 2024
10:00 AM - 12:00 PM EST
Location: Exhibit Hall E, F & G

Introduction: Acute Respiratory Distress Syndrome (ARDS) is a severe form of lung injury characterized by fluid buildup in the alveolar space which compromises the alveolar capillary barrier. ARDS also causes an impairment in production of surfactant, the substance that lines alveoli to lower surface tension, leading to collapse of the alveoli. ARDS leads to pulmonary edema, arterial hypoxemia, and respiratory failure due to lung inflammation and low surfactant production. Treatments for ARDS include mechanical ventilation, which can cause damage to the lung, and inhaled treatments, however, these treatments do not address surfactant dysfunction. Currently, there are treatments for surfactant deficiency in infants but no inhaled treatments for adults with ARDS. This study aims to quantify the effect of surfactant treatment on protein infiltration in the lungs when aerosolized dry powder surfactant is used to treat lipopolysaccharide (LPS) induced ARDS.

Materials and

Methods: Sprague Dawley rats weighing 350-450 g (males) or 300-350 g (females) were anesthetized using ketamine/xylazine (80 mg/kg, 8 mg/kg) and were dosed according to experimental group with 2.5 ymg/kg LPS in 0.5 mL/kg of 0.9% saline solution or 0.9% saline alone. Rats recovered for 24 hours then were anesthetized similarly and sham intubated or dosed with 5 mg novel surfactant dry powder aerosol, a spray-dried excipient enhanced growth formulation of synthetic phospholipid surfactant. Surfactant was administered via a novel air-jet dry powder insufflator as previously described by Pangeni et al (2023). Dosing was performed with a custom engineered rodent dry powder inhaler. The rats recovered for an additional 24 hours then measurements of lung mechanics, arterial and venous blood, bronchoalveolar lavage (BAL) fluid, and fixed and frozen lung tissue were obtained. Arterial blood was analyzed for blood gas measurements, BAL fluid was analyzed for protein content and inflammatory cell infiltration, and lung histology was performed to examine inflammation in tissue.

Results, Conclusions, and Discussions: Protein analysis of BAL fluid shows a trend toward higher total protein levels in the positive control group. This increase is ameliorated with surfactant treatment, but there is no statistically significant change. Blood gas data shows decreased hypoxia with surfactant treatment and novel air-jet device improves deposition of dry powder surfactant. Results from protein analysis display that surfactant decreases protein infiltration in the alveolar space when compared to positive control. This indicates that surfactant treatment may produce an anti-inflammatory effect. Further studies may include efficacy experiments that include BALF protein and cytology analysis, blood gas analysis, lung histology examination, and administering an increased number of surfactant doses to the animals over a longer timeline.

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