Neonatal hyperoxia exposure induces aortic biomechanical alterations and cardiac dysfunction in juvenile rats

Prolonged neonatal oxygen exposure causes persistent aortic structural and biomechanical alterations, which was even more pronounced after recovery in normoxia. This was accompanied by a marked impairment in left ventricular function. These findings have important implications as it suggests that premature babies exposed to oxygen may be predisposed to vascular dysfunction, leading to increased risk of cardiovascular disease in later life. As this affected population begins to age, there will be a critical need to identify the underlying pathophysiological mechanisms for these vascular morbidities in preterm survivors. AbstractSupplemental oxygen (O2) therapy in preterm infants impairs lung development, but the impact of O2 on long ‐term systemic vascular structure and function has not been well‐explored. The present study tested the hypothesis that neonatal O2 therapy induces long ‐term structural and functional alterations in the systemic vasculature, resulting in vascular stiffness observed in children and young adults born preterm. Newborn Sprague‐Dawley rats were exposed to normoxia (21% O2) or hyperoxia (85% O2) for 1 and 3  weeks. A subgroup exposed to 3 weeks hyperoxia was recovered in normoxia for an additional 3 weeks. Aortic stiffness was assessed by pulse wave velocity (PWV) using Doppler ultrasound and pressure myography. Aorta remodeling was assessed by collagen deposition and expression. Left ventricular (L V) function was assessed by echocardiograph...
Source: Physiological Reports - Category: Physiology Authors: Tags: ORIGINAL RESEARCH Source Type: research