PT - JOURNAL ARTICLE AU - Vanessa Zambelli AU - Laura Rizzi AU - Letizia Zucca AU - Anna Sigurtà AU - Paolo Delvecchio AU - Elena Bresciani AU - Antonio Biagio Torsello AU - Giacomo Bellani TI - Angiotensin-(1-7) effects in a rat model of ventilator-induced diaphragmatic dysfunction (VIDD) AID - 10.1183/1393003.congress-2017.OA300 DP - 2017 Sep 01 TA - European Respiratory Journal PG - OA300 VI - 50 IP - suppl 61 4099 - http://erj.ersjournals.com/content/50/suppl_61/OA300.short 4100 - http://erj.ersjournals.com/content/50/suppl_61/OA300.full SO - Eur Respir J2017 Sep 01; 50 AB - Introduction: Ventilator-induced diaphragmatic dysfunction (VIDD) is a frequent event during mechanical ventilation. Recent data show that renin-angiotensin system is involved in diaphragmatic skeletal muscle atrophy after mechanical ventilation (Kwon, O.S. et al. J Appl Physiol 119:1033-41).Aims: We evaluated the effects of the treatment with Angiotensin-(1-7) [Ang-(1-7)] in a rat model of VIDD. Moreover we verified if the administration of A-779, natural antagonist of Ang-(1-7) receptor, reverted the effects.Methods: Rats underwent prolonged mechanical ventilation (8 hours), while receiving continuously iv sterile saline 0.9% (Vehicle) or Ang-(1-7) or A-779 treatment. At the end, rats were sacrificed and diaphragm removed for ex vivo diaphragmatic contractility measurement (with electric stimulation), histological analysis and quantitative real-time polymerase chain reaction for Myogenin mRNA levels analysis.Results: As shown in the table, muscular fibers cross sectional area were higher and Myogenin mRNA levels were lower in Ang-(1-7) group. Diaphragmatic contractility did not differ. Diaphragmatic contractility (N/cm2)Cross Sectional Area in muscular fibers (µm2)Myogenin mRNA levels (ratio to b-actin)Vehicle4.94 ± 3.312426 ± 3977.02 ± 3.02Ang-(1-7)6.19 ± 3.332990 ± 760 *2.44 ± 1.22 *A-7794.49 ± 2.392612 ± 5506.81 ± 4.78*p<0.05 vs VehicleConclusions: Systemic treatment with Angiotensin-(1-7) during prolonged mechanical ventilation seemed to ameliorate the diaphragmatic function, probably due to the maintenance of the muscular fibers anatomy. This action appears mediated by the Mas receptor, whose blockade reverted the beneficial effects of Ang (1-7).