A total of 12.6% of young adults who were born very preterm and/or with a very low birth weight had moderate or severe problems in cognitive or neurosensory functioning. Compared with the general Dutch population, twice as many young adults who were born very preterm and/or with a very low birth weight were poorly educated, and 3 times as many were neither employed nor in school at age 19.

Two patients with incomplete pentalogy of Cantrell are described. The first was a girl with a large omphalocele with evisceration of the heart, liver and intestines with an intact sternum. Echocardiography showed profound intracardiac defects. The girl died 33 h after birth. The second patient was a female fetus with ectopia cordis (EC) without intracardiac anomalies; a large omphalocele with evisceration of the heart, stomach, spleen and liver; a hypoplastic sternum and rib cage; and a scoliosis. The pregnancy was terminated.

In a randomized controlled trial David van der Ham and colleagues investigate induction of labor versus expectant management for women with preterm prelabor rupture of membranes.

The fetus develops cardiovascular adaptations to protect vital organs in situations such as hypoxia and asphyxia. These include bradycardia, increased systemic blood pressure and redistribution of the cardiac output. The extent to which they involve maternal or placenta influences is not known. The objective of the present work was to study the cardiac output distribution in response to hypoxia in the chick embryo, which is independent of the mother. Fertilized eggs were studied at three incubation times (10‐13 days, 14‐16 days and 17‐19 days of a normal incubation time of 21 days). Eggs were placed in a Plexiglass box in which the oxygen concentration could be changed. Eggs were opened at the air cell and a chorioallantoic vein was catheterized. Cardiac output distribution was measured with 15 μm fluorescent microspheres injected during normoxia, during the last minute of a 5 min period of hypoxia and after 5 min of subsequent reoxygenation. Hypoxia caused a redistribution of the cardiac output in favour of heart (+17 to +160 % of baseline) and brain (+21 to +57 % of baseline) at the expense of liver (‐3 to ‐65 % of baseline), yolk‐sac (‐46 to ‐77 % of baseline) and carcass (‐6 to ‐33 % of baseline). The magnitude of the changes in cardiac output distribution to the heart, brain, liver and carcass in response to hypoxia increased with advancing incubation time. The data demonstrate the development of a protective redistribution of the cardiac output in response to hypoxia in the chick embryo from day 10 of incubation.

No abstract

In the mammalian fetus, the cardiovascular responses to acute hypoxaemia include a redistribution of the cardiac output away from the periphery towards the adrenal, myocardial and cerebral circulations. A component of the peripheral vasoconstriction is mediated by increased release of catecholamines into the fetal circulation during acute hypoxaemia. Previously, we have shown that the chick embryo also shows an increase in peripheral vascular resistance during acute hypoxaemia and that this response becomes progressively larger towards the end of the incubation period. However, the ontogeny of the catecholaminergic response to acute hypoxaemia has not been investigated in this species. Fertilised chicken eggs were studied on days 10, 13, 16 and 19 of incubation (hatching is at 21 days). At each stage of incubation, blood samples were obtained from the chorioallantoic artery of the chick embryos during normoxia and after 5 min of hypoxaemia for measurement of plasma concentrations of adrenaline and noradrenaline by HPLC. Basal plasma adrenaline and noradrenaline concentrations by the end of the incubation period were much higher in the chick embryo than values reported for mammalian fetuses during late gestation. During normoxia, basal plasma noradrenaline concentration remained unchanged during development but plasma adrenaline concentration showed a developmental increase from < 25.1 pmol l−1 at day 10 to 3 nmol l−1 at day 19 of incubation. Acute hypoxaemia caused an increase in plasma noradrenaline and adrenaline from day 13 and day 16 of incubation, respectively. In addition, the increase in plasma adrenaline and noradrenaline and in the ratio of plasma adrenaline to noradrenaline during acute hypoxaemia became progressively larger by the end of the incubation period. These data show an ontogenic increase in basal plasma catecholamines and in the catecholaminergic response to acute hypoxaemia in the chick embryo during the last third of the incubation period.

In response to an acute hypoxemic insult, the mammalian fetus shows a redistribution of the cardiac output in favor of the heart and brain. Peripheral vasoconstriction contributes to this response and is partly mediated by the release of catecholamines. Two mechanisms of catecholamine release in the fetus are reported: 1) neurogenic sympathetic stimulation and 2) a nonneurogenic mechanism via a direct effect of hypoxemia on chromaffin tissues. In the present study, the effects of sympathetic blockade on plasma catecholamine release and cardiac output distribution in response to acute hypoxemia were studied in the chick embryo at different stages of incubation. Only at the end of the incubation period, sympathetic blockade markedly attenuated the increase in plasma catecholamine concentrations and resulted in a greater fraction of the cardiac output distributed to the carcass. However, these effects did not prevent a significant increase in cardiac output to the brain and heart during acute hypoxemia. These data imply that in the chick embryo the contribution of neurogenic mechanisms to the catecholaminergic response to acute hypoxemia becomes greater by the end of the incubation period. fetus; hexamethonium; hypoxia; catecholamines; avian HYPOXEMIA IN THE FETUS, resulting largely from placental dysfunction or umbilical blood flow impairment, has been postulated to be a major cause of neurological damage and neonatal morbidity (20,30). During gestation, fetal cardiovascular responses develop to maintain organ blood flow and minimize damage of sensitive tissues during episodes of hypoxemia (for review see Refs. 11,12,and 14). The mechanisms mediating the fetal cardiovascular response to hypoxemia are triggered by carotid chemoreceptor stimulation, which elicits bradycardia, hypertension, and a redistribution of the cardiac output in favor of the adrenal gland, the heart, and the brain (10). Neural sympathetic stimulation and endocrine vasopressor substances, such as catecholamines, contribute to peripheral vasoconstriction, prioritizing the fetal cardiac output away from the periphery to the more vital organs (11,12,14). Previous studies from our laboratory have demonstrated the importance of catecholamine release in the cardiovascular response to an episode of acute hypoxemia in the chick embryo. At the end of the incubation period, plasma concentrations of catecholamines increase markedly in response to acute hypoxemia (21), and treatment of the chick embryo with the ␣-adrenergic receptor antagonist phentolamine prevented the redistribution of the cardiac output away from the peripheral circulations (22).In fetal sheep (4, 5, 27) and neonatal rats (29), at least two mechanisms mediating catecholamine release in response to hypoxemia have been described. First, before functional innervation of the adrenal glands, hypoxemia may stimulate chromaffin cells directly to promote catecholamine release into the circulation. Second, after the establishment of innervation to the adrenal gland, hypoxemia may stimulate adren...

Fetal responses to acute hypoxemia include bradycardia, increase in blood pressure, and peripheral vasoconstriction. Peripheral vasoconstriction contributes to the redistribution of the cardiac output away from ancillary vascular beds toward myocardial, cerebral, and adrenal circulations. We investigated the effect of alpha-adrenergic receptor blockade on this fetal response. Fluorescent microspheres were used to measure cardiac output distribution during basal and hypoxemic conditions with and without phentolamine treatment. Phentolamine altered basal cardiac output distribution, indicating a basal alpha-adrenergic tone, but this was mainly noted at the earlier stages of incubation. During hypoxemia, phentolamine prevented vasoconstriction in the carcass. At day 19 of incubation, the percent cardiac output distributed to the carcass increased by 20% compared with a decrease in the control group by 17%. Phentolamine markedly attenuated the subsequent redistribution of the cardiac output toward the brain (from +102% in the control group to -25% in the phentolamine-treated group) and the heart (from +196% in the control group to +69% in the phentolamine-treated group). In the chick embryo, alpha-adrenergic mechanisms contribute to the maintenance of basal vascular tone and to the redistribution of the cardiac output away from the peripheral circulations toward the brain and heart during hypoxemic conditions.