Long-term hypoxia alters endocrine and physiologic responses to umbilical cord occlusion in the ovine fetus.

OBJECTIVE: This study was designed to determine the effect of umbilical cord occlusion (UCO) on fetal endocrine responses in the long-term hypoxemic (LTH) ovine fetus. METHODS: Pregnant ewes were maintained at high altitude (3820 m) from day 30 of gestation. Normoxic control and LTH fetuses were catheterized, and an inflatable occluder was placed on the umbilical cord at day 132 of gestation. In the LTH group, maternal oxygen tension was maintained at approximately 60 mmHg by nitrogen infusion through a maternal tracheal catheter. On day 137, two 5-minute UCOs were performed. On day 139, the study was repeated with a 10-minute UCO. RESULTS: Basal adrenocorticotropic hormone (ACTH) levels and peak responses to the first 5-minute UCO were not different between control and LTH fetuses (17.6 +/- 4.0 to 418.8 +/- 41.3 in controls, 25.7 +/- 4.0 to 530.0 +/- 93.0 pg/mL in LTH fetuses). A similar pattern was observed during the second UCO. Basal cortisol levels were similar in both groups. In response to UCO, a significant increase in cortisol was observed in both groups, but peak concentrations in the LTH group were significantly higher than those in the control group (23.9 +/- 4.8 versus 14.8 +/- 2.9 ng/mL, respectively, P <.05). The second occlusion also increased cortisol concentrations, but no differences were observed between groups. After the 10-minute UCO, the ACTH and cortisol responses were similar to the first 5-minute occlusion, with higher cortisol levels in the LTH fetuses. CONCLUSION: Despite similar ACTH responses to UCO, the cortisol response was greater in the LTH fetuses than in normoxic controls. LTH appears to result in enhanced adrenal sensitivity to a secondary stressor or altered cortisol metabolism.

Umbilical arterial pH in patients with cerebral palsy.

BACKGROUND: Umbilical arterial pH (UApH) in severe cerebral palsy (CP) is not fully understood. AIMS: This work aims to determine the relationship between fetal acidemia and clinical features of severe CP. STUDY DESIGN: A retrospective study design is used. SUBJECTS: A review was conducted unti1 April 2013 among 218 infants with CP diagnosed to be caused by antenatal and/or intrapartum conditions determined by the Japan Council for Quality Health Care. After excluding patients in whom the causes of CP were thought to be due to events after delivery, 168 infants born at over 34weeks of gestation that both Apgar score and UApH were measured were selected. OUTCOME MEASURES: Severe fetal acidemia was defined as a pH of less than 7.0. RESULTS: Six major factors were found to be associated with CP: placental abruption (A, n=42), traumatic delivery with an abnormal FHR pattern (B, n=29), an abnormal FHR pattern during labor (C, n=27), chorioamnionitis with an abnormal FHR pattern (D, n=17), an abnormal FHR pattern before labor (E, n=14), and cord prolapse (F, n=10). The UApH was less than 7.0 in 114 cases (67.9%) and more than 7.20 in 20 cases (11.9%). The UApH values were lowest in group A (median 6.7, 6.43-6.99) and highest in group E (7.18, 6.92-7.45). The distribution of the UApH values was significantly different in these groups. CONCLUSION: Placental abruption was a factor most associated with low pH. Even among the infants with severe CP, over 10% of patients exhibited a non-acidemic status at birth.

Long-term hypoxia alters ovine fetal endocrine and physiological responses to hypotension.

Exposure to long-term hypoxia (LTH) results in altered cortisol responses in the ovine fetus. The present study was designed to test the hypothesis that LTH alters adrenal responsiveness to fetal hypotension. Pregnant ewes were maintained at high altitude (3,820 meters) from day 30 of gestation. Normoxic control and LTH fetuses were catheterized on day 132 of gestation. In the LTH group, maternal Po(2) was maintained comparable to that observed at altitude ( approximately 60 mmHg) by nitrogen infusion through a tracheal catheter. On day 137, fetuses received a 5-h saline infusion followed by infusion of sodium nitroprusside to reduce fetal arterial pressure by 30-35% for 10 min. The study was repeated on day 139 of gestation with a continuous cortisol infusion (10 microg/min). Hypothalamic and pituitary tissues were collected from additional fetuses for assessment of glucocorticoid receptors. During the saline infusion in response to hypotension, plasma ACTH increased over preinfusion mean values in both groups (P < 0.05). Plasma cortisol concentrations increased in both groups concomitant with increased ACTH secretion. However, peak values in the LTH fetuses were significantly higher compared with controls (P < 0.05). During the cortisol infusion, the ACTH response was eliminated in both groups, with ACTH levels significantly lower in the LTH group (P < 0.05). Glucocorticoid receptor binding was not different between groups. These results demonstrate an enhanced cortisol response to hypotension in LTH fetuses that does not appear to be the result of an increase in negative feedback sensitivity of the hypothalamic-pituitary-adrenal axis.