Pregnancy

Intrauterine Growth Retardation in Endothelial Nitric Oxide Synthase-Deficient Mice Is Established from Early Stages of Pregnancy

Abstract
The current study aimed to determine effects of deficiencies in NOS3 on embryo and fetal development by in vivo non-invasive real-time ultrasonographic assessment of phenotypic changes in Nos3-knockout pregnant mice and their wild-type counterparts. From Day 4.5 of pregnancy onwards, embryonic vesicle diameters, crown-rump length and trunk diameter were obtained by serial scanning of 7 adult pregnant female mice, strain: B6.129P2-Nos3^tm1Unc/J, N9 generation backcrossing with C57BL/6J mice, homozygous for the disruption of the endothelial NOS gene (group Nos3^-/-) and 12 pregnant wild-type C57BL/6J mice (group Nos3^+/+). All the measurements increased in both genotypes throughout gestation. However, embryo length and width were significantly larger in Nos3^+/+ than in Nos3^-/- mice from Day 8.5, and both longitudinal and transverse diameters of the entire gestational sacs were larger in Nos3^+/+ mouse from Day 10.5. Assessment of the relative growth of embryos/fetuses and gestational annexes showed different patterns between Nos3^-/- and Nos3^+/+ mice. Throughout the pregnancy, the distance between the external limit of the gestational sac and the embryo in Nos3^+/+ mouse diminished, in longitudinal sections, or remained unaffected, in transversal sections. In Nos3^-/- mouse, both longitudinal and transversal curves were composed by a first period of significant increase (P < 0.005) in the difference between embryo and gestational vesicle measurement, from Days 5.5 to 14.5, and a second period from Day 14.5 of pregnancy in which the changes were not significant. The results demonstrate that the processes of fetal growth retardation in the Nos3^-/- mouse are established from early pregnancy stages.

Key words: Pregnancy • Conceptus • Early development • Nitric oxide • Knockout-mice

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