Perfusion index and its dynamic changes in preterm neonates with patent ductus arteriosus.

AIM: The perfusion index (PI) and its dynamic change during respiration, and supressed the plethysmographic variability index (PVI), are calculated from pulse oximetry, and these indexes were recently proposed for continuous and noninvasive assessment of peripheral perfusion in neonates. We aimed to assess the effect of patent ductus arteriosus (PDA) on PI and PVI, according to ductal Doppler flow pattern. METHODS: Forty-five neonates with median (Q25-75) gestational age (GA) and birthweight of 27 (25-28) weeks and 857 (750-1080) grams, respectively, were assessed prospectively using serial echocardiography and pulse oximetry during the first postnatal week. RESULTS: Perfusion index increased from 0.70 (0.50-1.05) at day 1 to 1.50 (1.0-2.00) at day 7 (p < 0.01) and was not influenced by ductal flow pattern. PVI was 22 (18-27) and did not vary during the study period but differed according to ductal flow pattern, with lower values in the growing and pulsatile groups compared with the pulmonary hypertension (p < 0.05), closing and closed groups (p < 0.01). CONCLUSIONS: Ductal persistence and flow pattern did not affect PI but did affect PVI in preterm neonates of less than 29 weeks of GA. Future studies are needed to establish the usefulness of PVI in the early detection and management of PDA in preterm neonates.

Modulating the Oxytocin System During the Perinatal Period: A New Strategy for Neuroprotection of the Immature Brain?

Oxytocin is a neurohypophysal hormone known for its activity during labor and its role in lactation. However, the function of oxytocin (OTX) goes far beyond the peripheral regulation of reproduction, and the central effects of OTX have been extensively investigated, since it has been recognized to influence the learning and memory processes. OTX has also prominent effects on social behavior, anxiety, and autism. Interaction between glucocorticoids, OTX, and maternal behavior may have long-term effects on the developmental program of the developing brain subjected to adverse events during pre and perinatal periods. OTX treatment in humans improves many aspects of social cognition and behavior. Its effects on the hypothalamic-pituitary-adrenal axis and inflammation appear to be of interest in neonates because these properties may confer benefits when the perinatal brain has been subjected to injury. Indeed, early life inflammation and abnormal adrenal response to stress have been associated with an abnormal white matter development. Recent investigations demonstrated that OTX is involved in the modulation of microglial reactivity in the developing brain. This review recapitulates state-of-the art data supporting the hypothesis that the OTX system could be considered as an innovative candidate for neuroprotection, especially in the immature brain.

Early, time-dependent disturbances of hippocampal synaptic transmission and plasticity after in utero immune challenge.

BACKGROUND: Maternal infection during pregnancy is a recognized risk factor for the occurrence of a broad spectrum of psychiatric and neurologic disorders, including schizophrenia, autism, and cerebral palsy. Prenatal exposure of rats to lipopolysaccharide (LPS) leads to impaired learning and psychotic-like behavior in mature offspring, together with an enduring modification of glutamatergic excitatory synaptic transmission. The question that arises is whether any alterations of excitatory transmission and plasticity occurred at early developmental stages after in utero LPS exposure. METHODS: Electrophysiological experiments were carried out on the CA1 area of hippocampal slices from prenatally LPS-exposed male offspring from 4 to 190 days old to study the developmental profiles of long-term depression (LTD) triggered by delivering 900 shocks either single- or paired-pulse (50-msec interval) at 1 Hz and the N-methyl-D-aspartate receptor (NMDAr) contribution to synaptic transmission. RESULTS: The age-dependent drop of LTD is accelerated in prenatally LPS-exposed animals, and LTD is transiently converted into a slow-onset long-term potentiation between 16 and 25 days old. This long-term potentiation depends on Group I metabotropic glutamate receptors and protein kinase A activations and is independent of NMDArs. Maternal LPS challenge also leads to a rapid developmental impairment of synaptic NMDArs. This was associated with a concomitant reduced expression of GluN1, without any detectable alteration in the developmental switch of NMDAr GluN2 subunits. CONCLUSIONS: Aberrant forms of synaptic plasticity can be detected at early developmental stages after prenatal LPS challenge concomitant with a clear hypo-functioning of the NMDAr in the hippocampus. This might result in later-occurring brain dysfunctions.