Maternal nutritional restriction during gestation impacts differently on offspring muscular and elastic arteries and is associated with increased carotid resistance and ventricular afterload in maturity.

Abstract

Intrauterine undernutrition could impact offspring left ventricle (LV) afterload and arterial function. The changes observed in adulthood could differ depending on the arterial type, pathway and properties studied. Aim: To analyze whether undernutrition during early and mid-gestation is associated with changes in cardiovascular properties in adulthood. Pregnant ewes were assigned to one of the two treatment groups: (1) standard nutritional offer (high pasture-allowance, HPA; n = 16) or (2) nutritional restriction (50-75% of control intake) from before conception until day 122 of gestation (≈85% term) (low pasture allowance, LPA; n = 17). When offspring reached adult life, cardiovascular parameters were assessed in conscious animals (applanation tonometry, vascular echography). Peripheral and aortic pressure, carotid and femoral arteries diameters, intima-media thickness and stiffness, blood flow, local and regional resistances and LV afterload were measured. Blood samples were collected. Parameters were compared before and after adjustment for nutritional characteristics at birth and at the time of the cardiovascular evaluation. Doppler-derived cerebral vascular resistances, mean pressure/flow ratio (carotid resistance) and afterload indexes were higher in descendants from LPA than in descendants from HPA ewes (p < 0.05). Descendants from LPA had lower femoral diameters (p < 0.05). Cardiovascular changes associated with nutritional restriction during pregnancy did not depend on the offsprings' nutritional conditions at birth and/or in adult life. Pregnant ewes that experienced undernutrition gave birth to female offspring that exhibited increased carotid pathway resistances (cerebral microcirculatory resistances) and LV afterload when they reached the age of 2.5 years. There were differences in the impact of nutritional deficiency on elastic and muscular arteries.