Cerebral and Adrenal Monoamine Metabolism in the Growth-Retarded Rat Fetus under Normoxia and Hypoxia
Cerebral and Adrenal Monoamine Metabolism in the Growth-Retarded Rat Fetus under Normoxia and Hypoxia
复制标题
常氧和缺氧条件下生长迟缓大鼠胎儿脑和肾上腺单胺代谢
DOI：
10.1203/00006450-199202000-00008
复制
发表时间：
1992
影响因子：
3.6
通讯作者：
T. Hedner
中科院分区：
文献类型：
--
作者：
M. Thordstein;T. Hedner
The effect of intrauterine growth retardation (IUGR) on cerebral and adrenal monoamine metabolism was studied in the fetuses of eight nulliparous rat dams after unilateral uterine artery ligation on d 18 of gestation. On d 22 (term = 23 d), four dams were subjected to normoxia and four to hypoxia (10% O2) for 58 min while their hemodynamics and blood gases were monitored. An inhibitor of L-aromatic-decarboxylase (3-hydroxybensylhydrazine) was infused to measure monoamine synthesis rate. After decapitation of the dam, fetuses were delivered by sectio, decapitated, and dissected at −5±C. The body, liver, forebrain, brainstem, and adrenal glands were weighed, and concentrations of monoamine precursors, transmitters, and metabolites were assessed in the three latter organs. The weights of liver and forebrain were reduced in fetuses with IUGR, whereas brainstem and adrenal weights were unaltered. Epinephrine content in adrenals was reduced in proportion to body weight under normoxia but failed to increase under hypoxia as it did in appropriately grown fetuses. There were only minor changes in monoamine metabolism in the brainstem. In the forebrain, however, marked changes were seen, mainly in serotonin metabolism: under normoxia, fetuses with IUGR had decreased levels of serotonin and its metabolite 5-hydroxyindole acetic acid. Under hypoxia, appropriately grown fetuses reduced their concentrations of these substances, whereas fetuses with IUGR paradoxically increased their synthetic activity. It is concluded that a disturbance of central nervous serotonin metabolism prevails in growth-retarded rat fetuses in late gestation and that this disturbance depends on the degree of growth retardation and the degree of perinatal stress.
围产期可卡因暴露刺激大脑代谢。
影响因子：
2.9
作者：
Dow-Edwards,DL;Freed,LA;Milhorat,TH
通讯作者：
Milhorat,TH