Abstract
Objective. Meconium aspiration induces acute lung injury (ALI) in neonates born through meconium-stained amniotic fluid. As yet, there is no specific therapy for improving the outcome. Recently, angiotensin-converting enzyme 2 (ACE2), which inactivates angiotensin II (Ang II), has been shown to ameliorate murine ALI. Design. To evaluate the therapeutic potential of this substance, we studied ACE2 in a piglet model of ALI induced by meconium aspiration. Subjects. Twelve anesthetized piglets were subjected in an animal research laboratory. ALI was induced by tracheal meconium instillation. Thereafter, six animals were randomly assigned to the ACE2 group, while another 6 served as control. Measurements. Systemic, pulmonary hemodynamic, and blood gas exchange parameters and Ang II levels were examined before ALI induction and at various time points after administering ACE2 or saline. In addition, ventilation-perfusion distribution of the lung was assessed by the multiple inert gas elimination technique (MIGET). Main Results. Animals treated with ACE2 maintained significantly higher arterial partial pressures of oxygen (Pao2) and lower arterial partial pressures of carbon dioxide (Paco2), respectively. Furthermore, Ang II, which was substantially increased, returned to basal values. Conclusion. In summary, ACE2 improves blood gas exchange in meconium-induced ALI in piglets.
Highlights
In neonates, aspiration of meconium causes acute lung injury (ALI) and may lead to severe acute respiratory distress syndrome (ARDS), often associated with persistent fetal circulation [1, 2]
We recently showed that angiotensin-converting enzyme 2 (ACE2) ameliorates failure of oxygenation in a piglet model of lung injury induced by lipopolysaccharide (LPS) [8]
We investigated the potential influence of ACE2 on respiratory and hemodynamic parameters in a piglet model following meconium aspiration
Summary
Aspiration of meconium causes acute lung injury (ALI) and may lead to severe acute respiratory distress syndrome (ARDS), often associated with persistent fetal circulation [1, 2]. Similar to the situation in adults, neonates with ARDS require supportive intensive care including aggressive mechanical ventilation, circulatory support by catecholamines, and, in most severe cases, extracorporeal membrane oxygenation. ACE2 protects wild type mice from severe lung injury induced by acid aspiration, colon ligation, or endotoxin shock, and ACE2-knockout mice are more susceptible to these forms of lung disease as compared to wild type animals [7]. We recently showed that ACE2 ameliorates failure of oxygenation in a piglet model of lung injury induced by lipopolysaccharide (LPS) [8]
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