Maria Delivoria-Papadopoulos

A randomized clinical trial of early hospital discharge and home follow-up of very-low-birth-weight infants

To determine the safety, efficacy, and cost savings of early hospital discharge of very-low-birth-weight infants (less than or equal to 1500 g), we randomly assigned infants to one of two groups. Infants in the control group (n = 40) were discharged according to routine nursery criteria, which included a weight of about 2200 g. Those in the early-discharge group (n = 39) were discharged before they reached this weight if they met a standard set of conditions. For families of infants in the early-discharge group, instruction, counseling, home visits, and daily on-call availability of a hospital-based nurse specialist for 18 months were provided. Infants in the early-discharge group were discharged a mean of 11 days earlier, weighed 200 g less, and were two weeks younger at discharge than control infants. The mean hospital charge for the early-discharge group was 27 percent less than that for the control group (

Cellular mechanisms of hypoxic injury in the developing brain

47,520 vs.

Postnatal Changes in Oxygen Transport of Term, Premature, and Sick Infants: The Role of Red Cell 2,3-Diphosphoglycerate and Adult Hemoglobin

64,940; P less than 0.01), and the mean physicians charge was 22 percent less (

Red-Cell 2,3-Diphosphoglycerate Levels in Subjects with Chronic Hypoxemia

5,933 vs.

Lipid peroxidation as the mechanism of modification of the affinity of the Na+, K+-ATPase active sites for ATP, K+, Na+, and strophanthidin in vitro

7,649; P less than 0.01). The mean cost of the home follow-up care in the early-discharge group was

Lipid peroxidation in developing fetal guinea pig brain during normoxia and hypoxia.

576, yielding a net saving of

Gaseous Exchange and Acid-Base Balance in Premature Lambs during Liquid Ventilation since Birth

18,560 for each infant. The two groups did not differ in the numbers of rehospitalizations and acute care visits, or in measures of physical and mental growth. We conclude that early discharge of very-low-birth-weight infants, with follow-up care in the home by a nurse specialist, is safe and cost effective.

Protective effect of MgSO4 infusion on NMDA receptor binding characteristics during cerebral cortical hypoxia in the newborn piglet

The susceptibility of the developing brain to hypoxia should depend on the lipid composition of the brain cell membrane; the rate of lipid peroxidation; the presence of antioxidant defenses; and the development and modulation of the excitatory neurotransmitter receptors such as the N-methyl-D-aspartate (NMDA) receptor, the intracellular Ca++ and intranuclear Ca++-dependent mechanisms. In addition to the developmental status of these cellular components, the response of these potential mechanisms to hypoxia determines the fate of the hypoxic brain cell in the developing brain. In the fetal guinea pig and newborn piglet models, studies have demonstrated that brain tissue hypoxia results in brain cell membrane damage as evidenced by increased membrane lipid peroxidation and decreased Na+,K+-ATPase activity. Using electron spin resonance spectroscopy of alpha-phenyl-N-tert-butyl-nitrone spin-adducts, studies from our laboratory have demonstrated that tissue hypoxia results in increased free radical generation in the cortex of fetal guinea pigs and newborn piglets. We have also shown that brain tissue hypoxia modifies the N-methyl-D-aspartate receptor-ion channel, recognition and modulatory sites. Furthermore, a higher increase in NMDA receptor agonist-dependent Ca++ in synaptosomes of hypoxic as compared to normoxic fetuses was demonstrated. The increase in intracellular Ca++ may activate several enzymatic pathways such as phospholipase A2 and metabolism of arachidonic acid by cyclooxygenase and lipoxygenase, conversion of xanthine dehydrogenase to xanthine oxidase by proteases and activation of nitric oxide synthase. Using specific inhibitors of each of these enzymes such as cyclooxygenase (indomethacin), lipoxygenase (nordihydroguaiaretic acid), xanthine oxidase (allopurinol) and nitric oxide synthase (N-nitro-L-arginine), studies have shown that these enzyme reactions result in oxygen free radical generation, membrane lipid peroxidation and cell membrane dysfunction in the hypoxic brain. We suggest that, during hypoxia, the increased intracellular Ca++ may lead to an increased intranuclear Ca++ concentration and alter nuclear events including transcription of specific genes responsible for programmed cell death. In view of the developmental studies presented, the susceptibility of the fetal brain to hypoxia appears to increase with brain development as gestation approaches term.

Expression of Bax and Bcl-2 proteins during hypoxia in cerebral cortical neuronal nuclei of newborn piglets: effect of administration of magnesium sulfate.

Extract: In view of previous studies which did not show a precise relation between the percentage fetal hemoglobin and the position of the oxygen hemoglobin equilibrium curve, this problem was reexamined taking into account both the concentration of fetal hemoglobin and the 2,3-diphosphoglycerate (2,3-DPG) content of the cell.Forty-eight normal infants weighing 2500 g or more at birth were studied on days 1 and 5 of life and then at 3 and 6–9 weeks, and at 3–4, 5–6, and 8–11 months of age. Fifty-six ingfants ranging in birth weight from 900 to 2420 g were studied during the first 8 days of life and then at 2− to 3-week intervals until approximately 16 weeks of life. Twelve premature infants who were ill with the respiratory distress syndrome were also studied.Laboratory procedures consisted of measurement of total hemoglobin, fetal hemoglobin, red cell 2,3-DPG, and oxygen equilibrium curves.The “functioning DPG fraction” in millimicromoles per milliliter red blood cells (RBC) was obtained by multiplication of the total red cell DPG content (millimicromoles per milliliter RBC) by the percentage of adult hemoglobin.These studies confirm previous observations that the term infant begins life with blood that has an increased affinity for oxygen. During the first few months of life the oxygen-hemoglobin equilibrium curve gradually shifts to the right and between 4 and 6 months of age becomes similar to that observed in the normal adult.The change in P60 in these infants correlated neither with the change in red cell DPG content alone nor with the decline in fetal hemoglobin alone. Instead, the progressive decrease in oxygen affinity during the first 6 months of life correlated significantly (r = 0.876, P < 0.001) with the functioning DPG fraction. The term “functioning DPG fraction” is suggested to reflect the fact that both the DPG concentration and the adult hemoglobin concentration within the cell, with which the DPG interacts, are necessary factors in determining the position of the oxygen equilibrium curve.Infants with respiratory distress appear to have P50 s that are lower than those of healthy infants of similar gestational age and birth weight. This appears to be primarily a result of a decrease in red cell DPG concentration. It is this type of infant who may benefit from exchange transfusion with fresh adult blood.

The effects of deoxygenation of adult and fetal hemoglobin on the synthesis of red cell 2,3-diphosphoglycerate and its in vivo consequences

Recently, Benesch et al.1 , 2 and Chanutin and Curnish3 demonstrated that the affinity of a hemoglobin solution for oxygen may be decreased by its interaction with organic phosphates. Both 2,3-diph...