FETAL SHEEP ENDOCRINE RESPONSES TO SUSTAINED HYPOXEMIC STRESS AFTER CHRONIC FETAL-PLACENTAL EMBOLIZATION

Citation
R. Gagnon et al., FETAL SHEEP ENDOCRINE RESPONSES TO SUSTAINED HYPOXEMIC STRESS AFTER CHRONIC FETAL-PLACENTAL EMBOLIZATION, American journal of physiology: endocrinology and metabolism, 35(5), 1997, pp. 817-823
Citations number
25
Categorie Soggetti
Physiology
ISSN journal
01931849
Volume
35
Issue
5
Year of publication
1997
Pages
817 - 823
Database
ISI
SICI code
0193-1849(1997)35:5<817:FSERTS>2.0.ZU;2-H
Abstract
The purpose of this study was to determine the endocrine and circulato ry responses of the ovine fetus, near term, to sustained hyperemic str ess superimposed on chronic hypoxemia. Fetal sheep were chronically em bolized (n = 7) for 10 days between 0.84 and 0.91 of gestation via the descending aorta until arterial oxygen content was decreased by simil ar to 30%. Control animals (n = 8) received saline only. On experiment al day 10, both groups were embolized over a 6-h period until fetal ar terial pH decreased to similar to 7.00. Regional distribution of lower body blood flows was measured on day 10, before and at the end of acu te embolization. On day 10, the chronically embolized group had lower arterial oxygen content (P < 0.05), Po-2 (P < 0.01), and placental blo od flow (P < 0.05) than controls and higher prostaglandin E-2 (PGE(2)) and norepinephrine plasma concentrations (both P < 0.05). In response to a superimposed sustained hypoxemic stress, there was a twofold gre ater increase in PGE(2) in the chronically embolized group than in the control group (P < 0.05). However, the increase in fetal plasma corti sol in response to superimposed hypoxemic stress was similar in both g roups, despite significantly lower adrenocorticotropic hormone and adr enal cortex blood flow responses in the chronically hypoxemic group (b oth P < 0.05). We conclude that PGE(2) response to a sustained superim posed reduction in placental blood flow, leading to metabolic acidosis , is enhanced under conditions of chronic hypoxemia and may play an im portant role for the maintenance of the fetal cortisol response to an episode of superimposed acute stress.