Low Blood Pressure among Very-low-birth-weight Infants with Fetal Vessel Inflammation

Yanowitz, Toby; Baker, Robyn; Roberts, James M.; Brozanski, Beverly

doi:10.1038/sj.jp.7211091

Cited by 42 publications

(26 citation statements)

References 23 publications

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“…Previous reports have suggested a possible association between infection/inflammation, hypotension, and impaired cerebral vasoregulation (18,19). However, we found no association between indicators of maternal or placental infection and either cerebral pressure-passivity or hypotension.…”

Section: Discussioncontrasting

confidence: 56%

Fluctuating Pressure-Passivity Is Common in the Cerebral Circulation of Sick Premature Infants

et al. 2007

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Cerebral blood flow pressure-passivity results when pressure autoregulation is impaired, or overwhelmed, and is thought to underlie cerebrovascular injury in the premature infant. Earlier bedside observations suggested that transient periods of cerebral pressure-passivity occurred in premature infants. However, these transient events cannot be detected reliably by intermittent static measurements of pressure autoregulation. We therefore used continuous bedside recordings of mean arterial pressure (MAP; from an indwelling arterial catheter) and cerebral perfusion [using the nearinfrared spectroscopy (NIRS) Hb difference (HbD) signal) to detect cerebral pressure-passivity in the first 5 d after birth in infants with birth weight Ͻ1500 g. Because the Hb difference (HbD) signal [HbD ϭ oxyhemoglobin (HbO2) Ϫ Hb] correlates with cerebral blood flow (CBF), we used coherence between MAP and HbD to define pressure-passivity. We measured the prevalence of pressurepassivity using a pressure-passive index (PPI), defined as the percentage of 10-min epochs with significant low-frequency coherence between the MAP and HbD signals. Pressure-passivity occurred in 87 of 90 premature infants, with a mean PPI of 20.3%. Cerebral pressure-passivity was significantly associated with low gestational age and birth weight, systemic hypotension, and maternal hemodynamic factors, but not with markers of maternal infection. Future studies using consistent serial brain imaging are needed to define the relationship between PPI and cerebrovascular injury in the sick premature infant. C erebral pressure autoregulation maintains CBF relatively constant despite changes over a range of systemic blood pressures known as the autoregulatory plateau (1). Conversely, when changes in blood pressure result in concordant changes in CBF, the cerebral circulation is deemed "pressure passive." Current understanding is that cerebral pressurepassivity develops when changes in blood pressure exceed the capacity of the intact cerebral autoregulatory system or when the system is impaired by illness, injury, or vasoactive medications. Cerebral pressure-passivity is considered a risk factor for cerebrovascular injury in the sick premature infant (2-4). The current study extends our earlier work (3) using bedside NIRS to measure continuously cerebrovascular responses to spontaneous fluctuations in blood pressure. In our previous studies, we observed that cerebral pressure-passivity may wax and wane over relatively short periods in premature infants. To study the fluctuating nature of cerebral pressure-passivity and quantify its prevalence over time, we developed a continuous recording and analysis system because previously described techniques using intermittent static measurements (5-7) would be unable to measure the prevalence of fluctuating cerebral pressure-passivity over the highest risk for brain injury in premature infants. The principal aim of this technique is to make quantitative measurements of the prevalence of cerebral pressure-passivity rather...

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Section: Discussioncontrasting

confidence: 56%

Fluctuating Pressure-Passivity Is Common in the Cerebral Circulation of Sick Premature Infants

et al. 2007

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“…The mild reduction on blood pressure in the LPS-treated group before occlusion in the present study is consistent with the finding of relatively lower blood pressure in preterm infants with chorioamnionitis (38,39). Interestingly, these studies suggest that chorioamnionitis was associated with no change in middle cerebral artery Doppler blood flow velocities, or cerebral oxygenation, although variability was attenuated (40).…”

Section: R801supporting

confidence: 81%

Acute on chronic exposure to endotoxin is associated with enhanced chemoreflex responses in preterm fetal sheep

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Drury

Muir

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Experimental and clinical evidence show that the cardiopulmonary and systemic circulations are adversely affected in preterm neonates exposed to intrauterine inflammation (2)(3)(4)(5). This is probably caused by inflammationinduced impairment in pulmonary and systemic vascular development and function (4,(6)(7)(8)(9)(10)(11). Consequently, affected infants are more likely to suffer from inflammation-induced pulmonary hypertension, chronic lung disease, and disrupted cerebral perfusion, resulting in cerebral injury and poor neurological outcome (2,4,5,12,13).…”

mentioning

confidence: 99%

Intrauterine inflammation alters cardiopulmonary but not cerebral hemodynamics during open endotracheal tube suction in preterm lambs

et al. 2013

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Background: Intrauterine inflammation adversely affects cardiopulmonary, systemic, and cerebral hemodynamics in preterm neonates, but its impact on responses to endotracheal tube (ETT) suction, known to affect hemodynamics, is unknown. We hypothesized that intrauterine inflammation would alter the cardiopulmonary and cerebral hemodynamic response to open ETT suction in preterm lambs. Methods: Chronically instrumented fetuses received intraamniotic lipopolysaccharide (LPS; to induce intrauterine inflammation) or saline at 118 d of gestation (term ~147 d). At 125 d of gestation, lambs were delivered and mechanically ventilated. Open ETT suction was performed 30 min after delivery. Pulmonary and cerebral arterial pressures and flows were recorded continuously. results: Intrauterine inflammation reduced pulmonary blood flow (PBF) and increased pulmonary vascular resistance (PVR) after preterm birth. PBF and left-ventricular output (LVO) increased during and immediately after ETT suction in both groups, but the values were higher in LPS-exposed lambs. Preductal oxygenation significantly decreased during ETT suction but to a greater extent in LPS-exposed lambs. Cerebral blood flow and systemic arterial pressure were increased by open ETT suction similarly in the two groups. conclusion: Intrauterine inflammation exacerbates the neonatal hemodynamic response to open ETT suction.

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Low Blood Pressure among Very-low-birth-weight Infants with Fetal Vessel Inflammation

Abstract: FVI and PVL are associated with reduced BP over the first week of life.

Cited by 42 publications

References 23 publications

Fluctuating Pressure-Passivity Is Common in the Cerebral Circulation of Sick Premature Infants

Fluctuating Pressure-Passivity Is Common in the Cerebral Circulation of Sick Premature Infants

Acute on chronic exposure to endotoxin is associated with enhanced chemoreflex responses in preterm fetal sheep

Intrauterine inflammation alters cardiopulmonary but not cerebral hemodynamics during open endotracheal tube suction in preterm lambs

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