Funding outcome

Late-onset neonatal sepsis is an infection in the blood of children occurring at least seventy-two hours after birth. Often, these children do not survive and those who do may be burdened with lifelong effects. This is partially due to oxidative stress (the body's inability to balance antioxidants with the production of reactive oxygen species) and the effects of inflammation (production of cytokines meant to protect against cell injury). Oxidative stress and inflammation are key factors that may negatively influence the development of blood vessels and may lead to long-term effects, such as high blood pressure (hypertension) in adulthood. Interestingly, males tend to have higher elevations of oxidative stress and inflammatory markers which may be a factor in the higher mortality in males compared to females. Here, we aim to develop a neonatal sepsis model of oxidative and inflammatory stress and to determine if this stress results in hypertension and enhanced susceptibility to sepsis in adulthood. We will examine oxidative and inflammatory markers in neonatal rats at one, three, and seven days post-sepsis induction and follow survivors into adulthood to reassess stress markers and examine vascular function. We anticipate observing vascular dysfunction (seen as hypertension) and impaired vascular response to sepsis compared to controls, with males experiencing worse outcomes. Our findings will contribute to a greater understanding of the effects of neonatal sepsis on vascular development and may result in a shift in treatment approach where we treat neonatal sepsis in the context of vascular dysfunction to prevent hypertension and improve survival of sepsis in adulthood.