Meconium Aspiration Syndrome in Animal Models: Inflammatory Process, Apoptosis, and Surfactant Inactivation

SIMPLE SUMMARY: Meconium aspiration syndrome is a pathology that causes hypoxia, acidosis, and neonatal mortality. The mechanisms behind this rely on physiopathology and the interaction of meconium with pulmonary alveolar cells. The inflammatory response, inactivation of surfactant, and processes such as apoptosis or necrosis of alveolar macrophages, epithelial and endothelial cells also participate in this syndrome. In this review, the physiopathology of meconium aspiration syndrome will be discussed in veterinary medicine to understand the inflammatory response and the cellular and biochemical changes at the alveolar level that cause the main outcomes of this pathology. ABSTRACT: Meconium Aspiration Syndrome is a condition that causes respiratory distress in newborns due to occlusion and airway inflammation, and surfactant inactivation by meconium. This condition has been described in animal species such as canids, sheep, cattle, horses, pigs, and marine mammals. In its pathogenesis, the pulmonary epithelium activates a limited inflammatory response initiated by cytokines causing leukocyte chemotaxis, inhibition of phagocytosis, and pathogen destruction. Likewise, cytokines release participates in the apoptosis processes of pneumocytes due to the interaction of angiotensin with cytokines and the caspase pathway. Due to these reactions, the prevalent signs are lung injury, hypoxia, acidosis, and pneumonia with susceptibility to infection. Given the importance of the pathophysiological mechanism of meconium aspiration syndrome, this review aims to discuss the relevance of the syndrome in veterinary medicine. The inflammatory processes caused by meconium aspiration in animal models will be analyzed, and the cellular apoptosis and biochemical processes of pulmonary surfactant inactivation will be discussed.