Regional blood flow and the endocrine response to sustained hypoxemia in the preterm ovine fetus.
To determine the circulatory response of the preterm fetus to a sustained hypoxic insult, regional blood flow was measured (microsphere technique) in 12 unanesthetized fetal sheep (0.75 gestation) during a normoxic control period, after 1 h and 8 h of sustained hypoxemia, and after a 1-h recovery period. Associated endocrine changes which might relate to organ-specific changes in blood flow were also assessed. Myocardial and cerebral blood flow were increased by 240 and 90%, respectively, such that oxygen delivery to the heart was well maintained throughout the study, whereas that to the brain was significantly decreased by 8 h of hypoxic study. Regional blood flows for all structures within the brain showed similar percent increases, except that for the pituitary gland, where the increase was much smaller, and that for the choroid plexus, where blood flow actually fell. Whereas blood flow to upper body muscle showed no significant change throughout the study, that to the thyroid was increased by 70% by 1 h of hypoxic study but fell thereafter. Adrenal cortical blood flow relative to that of the medulla was increased 3-fold by 8 h of hypoxic study, indicating a differential effect of sustained hypoxia on these vascular beds. Although pituitary and thyroid blood flows showed no relationship to respective trophic and/or secretory hormones measured, values for adrenal cortical flow relative to medullary flow were well correlated with plasma concentrations of ACTH. It is concluded that the "centralization" of blood flow to vital organs in response to a sustained hypoxic insult is qualitatively similar for both the preterm and near term ovine fetus and that hypoxic regulatory mechanisms may be better protective of the heart. Additionally, a role for the functional activation of the adrenal gland in its blood flow response to sustained hypoxemia is suggested.
Richardson
B
B
Department of Obstetrics and Gynaecology, Lawson Research institute, University of Western Ontario, London, Canada.
Korkola
S
S
Asano
H
H
Challis
J
J
Polk
D
D
Fraser
M
M
D000138:Acidosis / Q000503:physiopathology; D000324:Adrenocorticotropic Hormone / Q000378:metabolism; D000818:Animals; D002560:Cerebrovascular Circulation / Q000502:physiology; D002908:Chronic Disease; D003326:Coronary Circulation / Q000502:physiology; D005315:Fetal Diseases / Q000503:physiopathology; D005865:Gestational Age; D006728:Hormones / Q000378:metabolism*; D006854:Hydrocortisone / Q000378:metabolism; D000860:Hypoxia / Q000503:physiopathology*; D012039:Regional Blood Flow; D012756:Sheep; D013972:Thyrotropin / Q000378:metabolism; D013974:Thyroxine / Q000378:metabolism
D006728:Hormones; D000324:Adrenocorticotropic Hormone; D013972:Thyrotropin; D013974:Thyroxine; D006854:Hydrocortisone