Search PubMed⌕ Search

Biomedical subjects

D Sadowsky

Publications and source records attributed to D Sadowsky.

67 records · Page 4Linked to original sources
PubMedDate not supplied

Activation of the fetal hypothalamic-pituitary-adrenal axis with prolonged and graded hypoxemia.

OBJECTIVE: The purpose of this study was to determine whether activation of the hypothalamic-pituitary-adrenal (HPA) axis and uteroplacental prostaglandin (PG) response occur before metabolic deterioration with a progressive decrease in fetal oxygenation. METHODS: Twenty-one chronically catheterized fetal sheep were studied between 126 and 135 days' gestation during a 24-hour normoxic control period and subsequently during 4 experimental days of either prolonged and graded hypoxemia, induced by progressively lowering the maternal inspired oxygen concentration (induced hypoxia, n = 12), or continued study on room air (control, n = 6; spontaneous hypoxia, n = 3). Fetal arterial blood was sampled daily for blood gases and pH, immunoreactive ACTH, cortisol, and PGE2. Placental cotyledons were obtained at the end of the experiment for measurement of prostaglandin-H synthase (PGHS) enzymatic activity. RESULTS: For all hypoxia group measurements, progressive reduction in fetal oxygenation resulted in little change in either plasma ACTH or cortisol until arterial O2 saturation was close to 30% with metabolic acidosis onsetting. This was in keeping with activation of the HPA axis at this time, because ACTH and cortisol values showed a strong linear correlation (r = 0.77, P < .01). Fetal plasma PGE2 concentrations and cotyledonary PGHS enzymatic activity, although somewhat higher in the hypoxia group animals, were not changed significantly. CONCLUSION: In response to prolonged and graded hypoxemia in the ovine fetus, activation of the HPA axis occurs only when the degree of hypoxemia is pronounced and close to that associated with metabolic deterioration, which may limit the time for any uteroplacental response and the ability to initiate labor.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

Effect of pulsatile intravenous oxytocin administration to pregnant sheep over the last third of gestation on fetal ACTH and cortisol responses to hypotension.

OBJECTIVE: To examine the effect of increasing myometrial contractility in the last third of gestation on ovine fetal response to hypotension. METHODS: Oxytocin (600 microU/kg/minute) or saline was infused via the maternal jugular vein as 5-minute pulses every 20 minutes, starting at 97 +/- 1 days of gestational age (mean +/- standard error of the mean) until labor. Fetal hypotension (10 minutes) was induced by intravenous nitroprusside infusion at 133 +/- 1 days' gestation. RESULTS: Ewes from both groups went into labor at the same gestational age. Total fetal body and adrenal gland weights were higher in controls than in the oxytocin-treated group. Maternal arterial pH and blood gas values were normal throughout the study. At 132-136 days' gestation, fetal arterial oxygen pressure was lower in the oxytocin group than in controls (P < .05). Basal fetal ACTH concentrations did not change between 130 and 136 days in both groups. The mean fetal plasma ACTH concentration was not different between the control (40.6 +/- 4.1 pg/mL) and oxytocin groups (32.6 +/- 4.9 pg/mL). Pre-hypotension fetal plasma ACTH was similar in both groups, whereas cortisol was lower in the oxytocin group. Hypotension significantly increased fetal plasma ACTH and cortisol concentrations; however, both ACTH and cortisol responses were smaller in the oxytocin group (P < .05). CONCLUSIONS: Increased myometrial contractility throughout the last third of gestation modifies the normal ACTH and cortisol relation at the critical time of prepartum increase in adrenocortical activity. In addition, fetal ACTH and cortisol responses to hypotension are diminished in fetuses exposed to such a prolonged increase in myometrial contractility. These observations support the hypothesis that myometrial contractility influences fetal neuroendocrine development.

Adrenocorticotropic Hormone↗