In collaboration with the Department of Pediatrics of the Oslo University Hospital lead by Ola D. Saugstad we are working on a well-established newborn piglet model of postnatal hypoxia. The model simulates neonatal asphyxia and allows us to examine systemic and regional hemodynamic changes during asphyxiation and re-oxygenation processes as well as the respective effects of the interventions. The use of pigs has advantages over other animals as its development is closer to the human fetus (36-38 weeks) with comparable body systems and weight (1.5-2kg) which allows the instrumentation and monitoring of the animal and controlling the confounding variables of hypoxia and hemodynamic derangements. This model is a valuable tool for studying brain damage and neurological impairments that may occur after hypoxia/ischemia (HI) in newborn piglets as well as other organ dysfunctions such as cardiac, pulmonar, renal and ocular disorders. The pathophysiology of the HI events seems to be mediated among others by reactive oxygen species (ROS) and oxidative stress, a deleterious situation that may be exacerbated by clinical situations like prematurity and also oxygen resuscitation.
We are working together with Saugstad’s group to investigate molecular mechanism beyond HI and searching for new biomarkers for predicting, diagnosing and monitoring HI as well as testing new therapies to prevent HI encephalopathy (HIE).
In addition, we established a piglet ocular model to investigate biochemical and molecular adaptive responses to acute postnatal hypoxia in retina and choroid. The immature brain of preterm newborns lacks vascular auto-regulation as compared to the term newborn and, therefore, both show different susceptibilities to hypoxic ischemic stress. In eye tissue, vascularization of the retina has oxygen dependent auto-regulation while choroid does not, therefore mimicking what happens in the adult vs the preterm brain.