thiobarbituric-acid and Fetal-Hypoxia

To detect a possible relationship between the increased vulnerability of the brain of the growth retarded fetus and lipid peroxidation, the activity of the latter was investigated in the forebrain of rat fetuses on day 22 of gestation (term = 23). Growth retardation was induced by uterine artery ligation on day 18. The susceptibility of the forebrain to lipid peroxidation was analysed using the thiobarbituric acid technique after exposure of the awake dams to room air or hypoxia (10% O2) for 58 minutes. Hemodynamics and blood gas status in the dams were stable under conditions of normoxia. When exposed to hypoxia, oxygen availability decreased and blood pressure fell slightly. When normalised for litter, lipid peroxidation covaried with fetal weight in fetuses from normoxic dams, only when Fe2+ (a promotor of lipid peroxidation) was added in the incubation. In fetuses from hypoxic dams, this relationship existed irrespective of whether Fe2+ was present during incubation. In all of these associations, smaller fetuses exhibited more intense lipid peroxidation. In the perinatal period, an increased vulnerability of the central nervous system prevails in growth retarded individuals. An increased tendency to undergo lipid peroxidation and/or a weak defence against this process may be part of the pathophysiologic background.

Topics: Animals; Brain; Female; Fetal Growth Retardation; Fetal Hypoxia; Lipid Peroxidation; Male; Rats; Rats, Inbred Strains; Thiobarbiturates