The development of diseases in later life, such as @entity2175 , @entity101 and @entity65 , is linked to abnormal intrauterine conditions that reduce birth weight. Obviously, fetal development can be disturbed so profoundly, that fetal programming is changed permanently. We have examined the effects of @entity519 , or more precisely @entity519 , on the fetal @entity2339 and lungs using molecular biology techniques in order to elucidate the underlying mechanisms. Chronically catheterized fetal @entity742 were subjected to a @entity519 (48 h) without change in arterial pH or pa @entity515 . Major changes occurred, although the degree of @entity519 was just moderate. There was a transient increase in the fetal plasma ACTH-concentrations with an upregulation of the @entity701 -concentrations, which was more pronounced in the older, hypoxemic fetuses (134-136 days of gestation) than in the younger, hypoxemic animals (126-130 days of gestation; term @entity29400 days). There was an unique, differential regulation for @entity57057 messenger RNA (mRNA), the precursor molecule of e.g. ACTH, in the pars distalis and pars intermedia of the pituitary gland. This finding supported the increased bioactivity besides the increased concentrations for ACTH. Simultaneously, there was an increase in the mRNAs of the @entity56184 and of the @entity134 -synthesizing enzymes in the fetal adrenal gland of the older, hypoxemic fetuses. No changes in the fetal plasma @entity2671 -concentrations were observed. Clearly, there was a selective increase of the @entity701 -synthesis. Growth and maturation of the fetal lung might also have been affected, because of the increase in surfactant-protein A mRNA in the older, hypoxemic animals and the decrease in the insulin-like growth factor-I and its binding protein-5 mRNA in the younger, hypoxemic fetuses. In summary, even a moderate degree of @entity519 was shown to affect the different levels of fetal organism profoundly, offering a pathophysiological basis for changes in fetal development.

Fetal hypoxemia on a molecular level: adaptive changes in the XXXX and the lungs.

@entity2175 :: ('MESH:D003924', 'Disease') :: ['diabetes type II'] @entity101 :: ('MESH:D006973', 'Disease') :: ['hypertension'] @entity742 :: ('9940', 'Species') :: ['sheep'] @entity515 :: ('CHEBI:29334', 'Chemical') :: ['CO2'] @entity134 :: ('CHEBI:35341', 'Chemical') :: ['steroid'] @entity519 :: ('MESH:D000860', 'Disease') :: ['hypoxemia', 'hypoxia'] @entity2339 :: ('MESH:D007029', 'Disease') :: ['hypothalamic-pituitary-adrenal (HPA) axis'] @entity57057 :: ('443212(Tax:9940)', 'Gene') :: ['pro-opiomelanocortin'] @entity701 :: ('MESH:D006854', 'Chemical') :: ['cortisol'] @entity29400 :: ('MESH:C082371', 'Chemical') :: ['is 145'] @entity56184 :: ('443482(Tax:9940)', 'Gene') :: ['ACTH-receptor'] @entity2671 :: ('MESH:D000735', 'Chemical') :: ['androstenedione'] @entity65 :: ('MESH:D002318', 'Disease') :: ['cardiovascular disease']
@entity2339 :: (MESH:D007029,Disease) :: ['hypothalamic-pituitary-adrenal (HPA) axis']
