INTRODUCTION: Preterm birth disrupts development of key components of the cardiovascular system, including the vasculature, leading to an increased risk of cardiovascular and cerebrovascular disease in adulthood. However, the long-term effects of late preterm birth on the vasculature remains unknown. We hypothesise that late preterm birth will result in region-dependent smooth muscle and endothelial dysfunction.
METHODS:Ewes were induced to deliver late preterm (132 days gestation) or at term (147 days gestation). Preterm lambs were administered antenatal betamethasone (2x11.4mg, 24hrs apart). Lambs were humanely killed at either 2 days (d, Term, n=11; Preterm, n=10) or 1 year of age (Term n=15; Preterm n=15) cerebral, coronary, mesenteric and renal small arteries (300-400μm diameter) were collected. Vascular function was assessed via wire myography to determine smooth muscle reactivity and endothelial vasodilator function.
RESULTS: Reactivity to vasoconstrictors and vasodilators was influenced by prematurity as well as by maturation, in a vascular-bed dependent manner. Effectiveness of the vasodilator nitric oxide (NO) remained constant throughout time and treatment in 3 of the vascular beds tested, except in the renal artery, in which it was halved at 1yr. Prostanoid was elevated in preterm mesenteric arteries at both 2d and 1yr. Relaxation attributed to endothelium-derived hyperpolarization (EDH) was significantly impaired in cerebral arteries of preterm lambs, while it was significantly reduced in mesenteric and coronary arteries at 1yr vs at 2d. In mesenteric and coronary arteries, reactivity to vasoconstrictors was enhanced in 2d preterm vs term offspring, an effect that was resolved at 1 year in mesenteric arteries.
CONCLUSION: Our findings demonstrate that some vascular beds are vulnerable to late preterm birth. In particular, altered cerebral function at one year may suggest a possible mechanism for the increased risk of stroke in preterm offspring