Effect of Transient Maternal Hypotension on Apoptotic Cell Death in Foetal Rat Brain

Abstract

Background:Intrauterine perfusion insufficiency induced bytran-sientmaternal hypotension hasbeenreported tobeassociated with foetal brain malformations. However, theeffects ofmaternal hypo-tension onapoptotic processes in thefoetal brain havenotbeenin-vestigated experimentally during the intrauterine period.Aims:Theaimof thisstudy wasto investigate theeffects of transient maternal hypotension onapoptotic celldeath in theintrauterine foetal brain. Study Design: Animal experimentation.Methods:Three-month-old female Wistar albino ratswereallocated intofourgroups (n=5each). Theimpact ofhypoxic/ischemic injury induced bytransient maternal hypotension onthe15thdayofpreg-nancy (lategestation) in ratswasinvestigated at 48(H17 group) or 96hours (H19 group) aftertheinsult. Control groups underwent the same procedure except forinduction ofhypotension (C17 andH17 groups). Brain sections ofonerandomly selected foetus from each pregnant ratwere histopathologically evaluated forhypoxic/isch-emic injury in themetencephalon, diencephalon, andtelencephalon byterminal transferase-mediated dUTP nickendlabelling andactive cysteine-dependent aspartate-directed protease-3 (caspase-3) positiv-ity for cell death. Results:Thenumber ofterminal transferase-mediated dUTP nick endlabelling (+)cells inalltheareas examined wascomparable inbothhypotension andcontrol groups. TheH17group hadactive caspase-3 (+)cellsin themetencephalon andtelencephalon, sparing diencephalon, whereas theC19andH19groups hadactive caspase-3 (+)cellsin allthreeregions. Thenumber of active caspase-3 (+)cells inthetelencephalon intheH19group washigher compared with themetencephalon anddiencephalon andcompared withH17group (p