The cerebral critical oxygen threshold of ventilated preterm lambs and the influence of antenatal inflammation

Chad Andersen, Jane Pillow, Andrew Gill, Beth Allison, Timothy Moss, Stuart Hooper, Ilias Nitsos, Martin Kluckow, Graeme Polglase

Research output: Contribution to journalArticleResearchpeer-review

Abstract

Perinatal inflammation is associated with adverse neurodevelopmental outcomes, which may be partly due to changes in the cerebral oxygen delivery/consumption relationship. We aimed to determine the critical oxygen delivery threshold of the brain of preterm, ventilated lambs and to determine whether the critical threshold is affected by exposure to inflammation in utero. Pregnant ewes received intra-amniotic injection of lipopolysaccharide or saline at 125 or 127 days of gestation. Pulmonary and systemic flow probes and catheters were surgically positioned in the fetus immediately before delivery at 129 days of gestation. After delivery, lambs were ventilated for 90 min using a positive end-expiratory pressure recruitment strategy. Cardio-respiratory variables and blood gases were measured regularly. Systemic and cerebral oxygen delivery, consumption (Fick), and extraction were calculated, and the relationship between cerebral delivery and consumption analyzed. Linear regression was used to define the transition or critical oxygen threshold as the point at which the slope of the oxygen delivery/consumption curve changed to be >10 degrees . Four subgroups were defined according to the calculated critical threshold. A total of 150 measurements were recorded in 18 lambs. Fetal cerebral oxygen consumption was increased by antenatal lipopolysaccharide (P <0.05). The postnatal critical oxygen threshold was 3.6 ml.kg(-1).min(-1), corresponding to cerebral oxygen consumption of 0.73 ml.kg(-1).min(-1). High oxygen delivery and consumption were associated with increased pulmonary and carotid blood flow and systemic extraction compared with low oxygen delivery and consumption. No postnatal effect of antenatal inflammation was observed. Inflammation in utero increases fetal, but not postnatal, cerebral oxygen consumption. Adverse alterations to pulmonary blood flow can result in reduced cerebral blood flow, oxygen delivery, and consumption. Regardless of exposure to inflammation, there is a consistent postnatal relationship between cerebral oxygen delivery and consumption.
Original languageEnglish
Pages (from-to)775 - 781
Number of pages7
JournalJournal of Applied Physiology
Volume111
Issue number3
DOIs
Publication statusPublished - 2011

Cite this

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title = "The cerebral critical oxygen threshold of ventilated preterm lambs and the influence of antenatal inflammation",
abstract = "Perinatal inflammation is associated with adverse neurodevelopmental outcomes, which may be partly due to changes in the cerebral oxygen delivery/consumption relationship. We aimed to determine the critical oxygen delivery threshold of the brain of preterm, ventilated lambs and to determine whether the critical threshold is affected by exposure to inflammation in utero. Pregnant ewes received intra-amniotic injection of lipopolysaccharide or saline at 125 or 127 days of gestation. Pulmonary and systemic flow probes and catheters were surgically positioned in the fetus immediately before delivery at 129 days of gestation. After delivery, lambs were ventilated for 90 min using a positive end-expiratory pressure recruitment strategy. Cardio-respiratory variables and blood gases were measured regularly. Systemic and cerebral oxygen delivery, consumption (Fick), and extraction were calculated, and the relationship between cerebral delivery and consumption analyzed. Linear regression was used to define the transition or critical oxygen threshold as the point at which the slope of the oxygen delivery/consumption curve changed to be >10 degrees . Four subgroups were defined according to the calculated critical threshold. A total of 150 measurements were recorded in 18 lambs. Fetal cerebral oxygen consumption was increased by antenatal lipopolysaccharide (P <0.05). The postnatal critical oxygen threshold was 3.6 ml.kg(-1).min(-1), corresponding to cerebral oxygen consumption of 0.73 ml.kg(-1).min(-1). High oxygen delivery and consumption were associated with increased pulmonary and carotid blood flow and systemic extraction compared with low oxygen delivery and consumption. No postnatal effect of antenatal inflammation was observed. Inflammation in utero increases fetal, but not postnatal, cerebral oxygen consumption. Adverse alterations to pulmonary blood flow can result in reduced cerebral blood flow, oxygen delivery, and consumption. Regardless of exposure to inflammation, there is a consistent postnatal relationship between cerebral oxygen delivery and consumption.",
author = "Chad Andersen and Jane Pillow and Andrew Gill and Beth Allison and Timothy Moss and Stuart Hooper and Ilias Nitsos and Martin Kluckow and Graeme Polglase",
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The cerebral critical oxygen threshold of ventilated preterm lambs and the influence of antenatal inflammation. / Andersen, Chad; Pillow, Jane; Gill, Andrew; Allison, Beth; Moss, Timothy; Hooper, Stuart; Nitsos, Ilias; Kluckow, Martin; Polglase, Graeme.

In: Journal of Applied Physiology, Vol. 111, No. 3, 2011, p. 775 - 781.

Research output: Contribution to journalArticleResearchpeer-review

TY - JOUR

T1 - The cerebral critical oxygen threshold of ventilated preterm lambs and the influence of antenatal inflammation

AU - Andersen, Chad

AU - Pillow, Jane

AU - Gill, Andrew

AU - Allison, Beth

AU - Moss, Timothy

AU - Hooper, Stuart

AU - Nitsos, Ilias

AU - Kluckow, Martin

AU - Polglase, Graeme

PY - 2011

Y1 - 2011

N2 - Perinatal inflammation is associated with adverse neurodevelopmental outcomes, which may be partly due to changes in the cerebral oxygen delivery/consumption relationship. We aimed to determine the critical oxygen delivery threshold of the brain of preterm, ventilated lambs and to determine whether the critical threshold is affected by exposure to inflammation in utero. Pregnant ewes received intra-amniotic injection of lipopolysaccharide or saline at 125 or 127 days of gestation. Pulmonary and systemic flow probes and catheters were surgically positioned in the fetus immediately before delivery at 129 days of gestation. After delivery, lambs were ventilated for 90 min using a positive end-expiratory pressure recruitment strategy. Cardio-respiratory variables and blood gases were measured regularly. Systemic and cerebral oxygen delivery, consumption (Fick), and extraction were calculated, and the relationship between cerebral delivery and consumption analyzed. Linear regression was used to define the transition or critical oxygen threshold as the point at which the slope of the oxygen delivery/consumption curve changed to be >10 degrees . Four subgroups were defined according to the calculated critical threshold. A total of 150 measurements were recorded in 18 lambs. Fetal cerebral oxygen consumption was increased by antenatal lipopolysaccharide (P <0.05). The postnatal critical oxygen threshold was 3.6 ml.kg(-1).min(-1), corresponding to cerebral oxygen consumption of 0.73 ml.kg(-1).min(-1). High oxygen delivery and consumption were associated with increased pulmonary and carotid blood flow and systemic extraction compared with low oxygen delivery and consumption. No postnatal effect of antenatal inflammation was observed. Inflammation in utero increases fetal, but not postnatal, cerebral oxygen consumption. Adverse alterations to pulmonary blood flow can result in reduced cerebral blood flow, oxygen delivery, and consumption. Regardless of exposure to inflammation, there is a consistent postnatal relationship between cerebral oxygen delivery and consumption.

AB - Perinatal inflammation is associated with adverse neurodevelopmental outcomes, which may be partly due to changes in the cerebral oxygen delivery/consumption relationship. We aimed to determine the critical oxygen delivery threshold of the brain of preterm, ventilated lambs and to determine whether the critical threshold is affected by exposure to inflammation in utero. Pregnant ewes received intra-amniotic injection of lipopolysaccharide or saline at 125 or 127 days of gestation. Pulmonary and systemic flow probes and catheters were surgically positioned in the fetus immediately before delivery at 129 days of gestation. After delivery, lambs were ventilated for 90 min using a positive end-expiratory pressure recruitment strategy. Cardio-respiratory variables and blood gases were measured regularly. Systemic and cerebral oxygen delivery, consumption (Fick), and extraction were calculated, and the relationship between cerebral delivery and consumption analyzed. Linear regression was used to define the transition or critical oxygen threshold as the point at which the slope of the oxygen delivery/consumption curve changed to be >10 degrees . Four subgroups were defined according to the calculated critical threshold. A total of 150 measurements were recorded in 18 lambs. Fetal cerebral oxygen consumption was increased by antenatal lipopolysaccharide (P <0.05). The postnatal critical oxygen threshold was 3.6 ml.kg(-1).min(-1), corresponding to cerebral oxygen consumption of 0.73 ml.kg(-1).min(-1). High oxygen delivery and consumption were associated with increased pulmonary and carotid blood flow and systemic extraction compared with low oxygen delivery and consumption. No postnatal effect of antenatal inflammation was observed. Inflammation in utero increases fetal, but not postnatal, cerebral oxygen consumption. Adverse alterations to pulmonary blood flow can result in reduced cerebral blood flow, oxygen delivery, and consumption. Regardless of exposure to inflammation, there is a consistent postnatal relationship between cerebral oxygen delivery and consumption.

UR - http://jap.physiology.org/content/111/3/775.full.pdf+html

U2 - 10.1152/japplphysiol.00214.2011

DO - 10.1152/japplphysiol.00214.2011

M3 - Article

VL - 111

SP - 775

EP - 781

JO - Journal of Applied Physiology

JF - Journal of Applied Physiology

SN - 8750-7587

IS - 3

ER -