Early Pulmonary Stress During Intra-Abdominal Hypertension and Hypervolemia: Surfactant Protein A1 and...

Conventional endpoints may overlook pulmonary biological stress during abdominal mechanical loading and volume expansion. This controlled experimental study evaluated whether intra-abdominal hypertension (IAH), hypervolemia (HV), or their combination induces early pulmonary biochemical, permeability, oxidative-ischemic, inflammatory, and structural responses, with particular focus on surfactant protein A1 (SP-A1). Thirty-five male Wistar rats were randomized to Sham, HV, IAH, or IAH + HV groups. IAH was induced by CO₂ pneumoperitoneum at 12-15 mmHg, and HV by 6% hydroxyethyl starch infusion until hematocrit decreased to approximately 25%; animals were followed for 120 min. Physiological variables, blood gases, wet-to-dry ratio, ATS-based histopathology, and biomarkers in plasma, bronchoalveolar lavage (BAL) fluid, and lung tissue were assessed. The dominant finding was a compartment-specific SP-A1 response: plasma SP-A1 was highest in the IAH group, whereas BAL fluid SP-A1 increased in both HV and IAH groups. These changes occurred without significant alterations in MAP, HR, SpO₂, wet-to-dry ratio, or ATS lung injury score. Permeability index was higher in HV-containing groups, and sialic acid and oxidative-ischemic markers showed compartment-dependent changes, whereas TNF-α, IL-6, HA, and ANP did not differ significantly. These exploratory, hypothesis-generating findings suggest that SP-A1 may reveal early pulmonary epithelial/barrier stress before overt physiological or structural injury becomes apparent.