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

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.

Pathophysiology of Perinatal Asphyxia in Humans and Animal Models.

Perinatal asphyxia is caused by lack of oxygen delivery (hypoxia) to end organs due to an hypoxemic or ischemic insult occurring in temporal proximity to labor (peripartum) or delivery (intrapartum). Hypoxic-ischemic encephalopathy is the clinical manifestation of hypoxic injury to the brain and is usually graded as mild, moderate, or severe. The search for useful biomarkers to precisely predict the severity of lesions in perinatal asphyxia and hypoxic-ischemic encephalopathy (HIE) is a field of increasing interest. As pathophysiology is not fully comprehended, the gold standard for treatment remains an active area of research. Hypothermia has proven to be an effective neuroprotective strategy and has been implemented in clinical routine. Current studies are exploring various add-on therapies, including erythropoietin, xenon, topiramate, melatonin, and stem cells. This review aims to perform an updated integration of the pathophysiological processes after perinatal asphyxia in humans and animal models to allow us to answer some questions and provide an interim update on progress in this field.