[Metabolic, cardiovascular and sympathoadrenal reactions of the fetus to progressive hypoxia--animal experiment studies].
During delivery a reduction of placental blood flow in relation to uterine contractions resulting in repetitive decelerations of the fetal heart rate is frequently encountered. In this context the question arises whether a critical threshold of oxygen saturation (SO2) in fetal arterial blood can be defined, below which a severe fetal acidosis and a fetal shock syndrome may develope. In chronically instrumented ewes (8 experiments) a slowly progressive fetal hypoxia was induced by stepwise reduction of uterine blood flow via occlusion of the maternal aorta. Fetal arterial blood pressure and heart rate were continuously monitored and fetal arterial blood samples were taken intermittently from a catheter placed in the fetal aorta. The stepwise decrease of fetal arterial SO2 was 10% at time intervals of 15-30 minutes. With SO2-values above 15%, lactate increased 0.01-0.03 mmol/l/min and the pH decreased 0.003-0.0012/min. A significant increase of lactate concentration (0.1-0.3 mmol/l/min) and decrease of the pH (0.003-0.009/min) was encountered when the fetal arterial SO2 was below 15%. With progressive desoxygenation systolic and diastolic blood pressure as well as pulse pressure increased. There was no uniform reaction pattern of the basal fetal heart rate to progressive hypoxia; while in some experiments tachycardia prevailed, bradycardia was encountered in other experiments. Plasma free catecholamines exhibited an inverse relationship to SO2 with an exponential increase of catecholamine concentrations when SO2 fell below 15-20%. During almost complete desoxygenation (SO2 below 5%), catecholamine concentrations were increased 100 fold (norepinephrine), 1000 fold (epinephrine) and 50 fold (dopamine) as compared to control values. In comparison to free catecholamines increases of the concentrations of cortisol and aldosterone were only small. The increase of cortisol with progressive hypoxia may explain the endogenous stimulation of lung maturity during fetal stress. Our experiments suggest that a SO2 level of 15-20% represents a critical threshold for development of severe fetal acidosis and a fetal shock syndrome. However, even during severe hypoxia (SO2 below 10%) the sheep fetus is able to maintain blood pressure for at least 30 minutes with the help of an excessive catecholamine secretion. Only with anoxia a breakdown of fetal circulation has to be anticipated within a few minutes.
D000136:Acid-Base Equilibrium; D000138:Acidosis / Q000503:physiopathology; D000450:Aldosterone / Q000097:blood; D000818:Animals; D001794:Blood Pressure; D002245:Carbon Dioxide / Q000097:blood; D002395:Catecholamines / Q000097:blood*; D005260:Female; D005311:Fetal Hypoxia / Q000503:physiopathology*; D006340:Heart Rate, Fetal; D006854:Hydrocortisone / Q000097:blood; D007773:Lactates / Q000097:blood*; D019344:Lactic Acid; D010100:Oxygen / Q000097:blood*; D011247:Pregnancy; D012756:Sheep; D012769:Shock / Q000503:physiopathology; D014590:Uterine Contraction
D002395:Catecholamines; D007773:Lactates; D002245:Carbon Dioxide; D019344:Lactic Acid; D000450:Aldosterone; D010100:Oxygen; D006854:Hydrocortisone
Metabolische, kardiovaskuläre und sympathoadrenale Reaktionen des Feten auf eine progrediente Hypoxie--Tierexperimentelle Untersuchungen.