Physiology of transition from intrauterine to extrauterine life
ABSTRACT The transition from fetus to newborn is the most complex adaptation that occurs in human experience. Lung adaptation requires coordinated clearance of fetal lung fluid, surfactant secretion, and onset of consistent breathing. The cardiovascular response requires striking changes in blood flow, pressures, and pulmonary vasodilation. Energy metabolism and thermoregulation must be quickly controlled. The primary mediators that prepare the fetus for birth and support the multiorgan transition are cortisol and catecholamine. Abnormalities in adaptation are frequently found following preterm birth or cesarean delivery at term, and many of these infants need delivery room resuscitation to assist in this transition.
- NeoReviews 06/2012; 13(6):e334-e335. DOI:10.1542/neo.13-6-e334
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ABSTRACT: Very low birth weight preterm newborns are susceptible to the development of debilitating inflammatory diseases, many of which are associated with chorioamnionitis. To define the effects of chorioamnionitis on the fetal immune system, IL-1b was administered intra-amniotically at ∼80% gestation in rhesus monkeys. IL-1b caused histological chorioamnionitis, as well as lung inflammation (infiltration of neutrophils or monocytes in the fetal airways). There were large increases in multiple proinflammatory cytokine mRNAs in the lungs at 24 h postadministration, which remained elevated relative to controls at 72 h. Intra-amniotic IL-1b also induced the sustained expression of the surfactant proteins in the lungs. Importantly, IL-1b significantly altered the balance between inflammatory and regulatory T cells. Twenty-four hours after IL-1b injection, the frequency of CD3+CD4+FOXP3+ T cells was decreased in lymphoid organs. In contrast, IL-17A–producing cells (CD3+CD4+, CD3+CD42, and CD32CD42 subsets) were increased in lymphoid organs. The frequency of IFN-g–expressing cells did not change. In this model of a single exposure to an inflammatory trigger, CD3+CD4+FOXP3+ cells rebounded quickly, and their frequency was increased at 72 h compared with controls. IL-17 expression was also transient. Interestingly, the T cell profile alteration was confined to the lymphoid organs and not to circulating fetal T cells. Together, these results suggest that the chorioamnionitis-induced IL-1/IL-17 axis is involved in the severe inflammation that can develop in preterm newborns. Boosting regulatory T cells and/or controlling IL-17 may provide a means to ameliorate these abnormalities.The Journal of Immunology 06/2013; 191(3). DOI:10.4049/jimmunol.1300270 · 5.36 Impact Factor
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ABSTRACT: Abstract Aim: To assess whether blood values of C-reactive protein (CRP) in healthy term newborns, are influenced by stress. Material and methods: Since different types of delivery [vaginal delivery (VD), emergency C-section (EMCS) and elective C- section (ELCS)] are notoriously characterized by different levels of stress for the baby, these three groups were used as models of different levels of stress. The mean CRP values of the three groups obtained in the first hours of life were compared. Results: We retrieved 1012 babies. Median values (3(rd)-97(th) ct) were: 0.05 (0.01-0.46), 0.17 (0.02-1.54), 0.30 (0.04-1.77), 0.43 (0.05-1.31), 0.40 (0.04-1.13) at 12, 24, 48, 72 and 96 hours respectively. Mean values in babies born after VD were statistically higher than those born after C-section, and higher CRP values were present in EMCS with respect to ELCS. Conclusion: This study described normal blood CRP values in a wide population of term babies. An influence of the type of delivery on blood CRP is evident, and this may be explained by the different amount of perinatal stress induced by anyone of the three types of delivery we considered.The journal of maternal-fetal & neonatal medicine: the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians 07/2013; 27(6). DOI:10.3109/14767058.2013.823937 · 1.21 Impact Factor