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404 Dspc-Palmitate Kinetic in A Model of Lung Unilateral Acid Injury
  1. G Lamonica1,
  2. L Vedovelli2,
  3. M Amigoni3,
  4. V Zambelli3,
  5. M Scanziani3,
  6. M Facco Marcazzò1,
  7. G Bellani3,
  8. PE Cogo4
  1. 1Department of Pediatrics
  2. 2Department of Pharmacology and Anesthesiology, University of Padua, Padova
  3. 3Experimental Medicine, University Milano-Bicocca, Monza
  4. 4Medical Cardiac and Cardiac Surgical Pediatrics, Bambino Gesù Children’s Hospital, IRCCS, Roma, Italy

Abstract

Aspiration of gastric (acid) content is a major cause of acute respiratory failure that occurs in children with severe gastroesophageal reflux, gastrointestinal malformations, and neurologic impairment. Alveolar surfactant alterations were demonstrated in diseases with similar aetiology like ARDS and meconium aspiration syndrome. To understand if the surfactant system is modulated locally or if an unilateral injury influences both lungs, we measured alveolar surfactant DSPC in a murine model of unilateral acid injury.

We developed a mouse model of acid lung injury confined in a single lung (right). Deuterated water was injected 18 h after the lung injury and DSPC-palmitate deuterium enrichment was measured for the next 24 hours in BAL and tissue. MPO and total protein analysis was performed separately to each lung to assess the inflammatory status.

Inflammatory status of both lungs was markedly increased in the injured (right) lung. DSPC content was not significantly different between the two lungs in tissue homogenates at all time points (1.83±0.3 vs. 1.75±0.6 umol/g of lung). Conversely, DSPC content in BAL was significantly increased in the not-injured lung (1.00±0.36 vs. 1.49±0.5 umol/g of lung, p=0.008). Fractional synthetic rates did not significantly change in both homogenates and BAL between the two lungs.

These preliminary data suggest that surfactant system is likely to be regulated at the whole lung level. The not-injured lung seems to increase the amount of DSPC in the alveolar space as a compensatory mechanism for the damage in the contralateral lung.

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