Pediatric research
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Chorioamnionitis is associated with increased lung and brain injury in premature infants. Ureaplasma is the microorganisms most frequently associated with preterm birth. Whether Ureaplasma-induced antenatal inflammation worsens lung and brain injury is unknown. ⋯ Antenatal inflammation exacerbates the deleterious effects of oxygen on lung development, but the broth effects prohibit concluding that UP by itself is a compounding risk factor for bronchopulmonary dysplasia. In contrast, antenatal UP-induced inflammation alone is sufficient to disturb brain development. This model may be helpful in exploring the pathophysiology of perinatal lung and brain injury to develop new protective strategies.
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Reduced cerebral function after neonatal hypoxia-ischemia is an early indicator of hypoxic-ischemic encephalopathy. Near-infrared spectroscopy offers a clinically relevant means of detecting impaired cerebral metabolism from the measurement of the cerebral metabolic rate of oxygen (CMRO2). The purpose of this study was to determine the relationship between postinsult CMRO2 and duration of hypoxia-ischemia in piglets. ⋯ In the first 4 h after the insult, average CMRO2 of the insult group was significantly depressed (33 +/- 3% reduction compared with controls) and by 8 h, a significant correlation developed, which persisted for the remainder of the study, between CMRO2 and the duration of ischemia. Histologic staining suggested little brain damage resulted from shorter insult durations and considerable damage from more prolonged insults. This study demonstrated that near-infrared spectroscopy could detect early changes in CMRO2 after hypoxia-ischemia for a range of insult severities and CMRO2 could be used to distinguish insult severity by 8 h after the insult.
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Oxygen is critical for multicellular existence. Its reduction to water by the mitochondrial electron transport chain helps supply the metabolic demands of human life. ⋯ In this review, we explore the mechanisms responsible for maintaining oxygen homeostasis and the consequences of their dysfunction. With an eye toward defining clinical care guidelines for the management of critically ill neonates, we present evidence describing the role of physiologic hypoxia during development and the adverse consequences of hyperoxia in-term as well as preterm infants.
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Antenatal inflammation is a known risk factor of bronchopulmonary dysplasia. The authors hypothesized that lipopolysaccharide (LPS) administration amplifies hyperoxia-induced lung injury in neonatal rats. LPS (0.5 or 1.0 microg) or normal saline was injected into the amniotic sacs of pregnant rats at 20 d gestation (term 22.5 d). ⋯ LPS at 1.0 microg independently induced modest lung injury and also amplified the effect of 1 wk of hyperoxia. However, this sensitizing effect of LPS was not observed in rats subjected to 2 wks of hyperoxia, which in itself caused extensive lung injury (possibly masking the effect of LPS). The authors concluded that intra-amniotic LPS sensitizes neonatal rat lungs, and thus, amplifies the hyperoxia-induced inhibition of alveolarization.
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In a prospective study, we monitored simultaneously left and right parieto-frontal-cerebral oxygen saturation (rScO2) and cerebral fractional tissue oxygen extraction (cFTOE) using near-infrared spectroscopy in 36 very preterm neonates during the first 3 d of life. Simple regression analysis showed a close correlation between left and right rScO2 (r = 0.89, p < 0.01) and cFTOE (r = 0.88, p < 0.01), respectively. ⋯ However, we found that during stable systemic oxygenation (i.e., arterial oxygen saturation [SaO2 between 85 and 97%]) the limits of agreement between left and right improved from -7.8 to +8.2% and -0.088 to +0.084 for rScO2 and cFTOE, respectively (all p < 0.05). We conclude that bilateral near-infrared spectroscopy-measured rScO2 and cFTOE can reveal differences up to 10% between left and right hemisphere, especially during unstable arterial saturations, which may indicate uneven cerebral oxygenation.