Cerebral blood flow and metabolism in relation to electrocortical activity with severe umbilical cord occlusion in the near-term ovine fetus

Kaneko, Masatoki; White, Susan; Homan, Jacobus; Richardson, Bryan

doi:10.1067/mob.2003.219

Cited by 45 publications

(51 citation statements)

References 17 publications

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“…In these experiments, as in another study in which the umbilical cord was occluded (22), plasma glucose concentrations were increased. Hypoxia-induced increases in adrenergic activity and plasma catecholamines increase plasma glucose concentrations in fetal sheep (21) and lead to increased plasma glucose concentrations through glycogenolysis (38).…”

Section: Discussionmentioning

confidence: 74%

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Changes in cerebral blood flow, cerebral metabolites, and breathing movements in the sheep fetus following asphyxia produced by occlusion of the umbilical cord

Yan¹,

Baburamani²,

Walker³

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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Severe global fetal asphyxia, if caused by a brief occlusion of the umbilical cord, results in prolonged cerebral hypoperfusion in fetal sheep. In this study, we sought evidence to support the hypothesis that cerebral hypoperfusion is a consequence of suppressed cerebral metabolism. In the 24 h following complete occlusion of the umbilical cord for 10 min, sagittal sinus blood flow velocity was significantly decreased for up to 12 h. Capillary blood flow, measured using microspheres, decreased at 1 and 5 h after cord occlusion in many brain regions, including cortical gray and white matter. Microdialysis probes implanted in the cerebral cortex revealed an increase in extracellular glucose concentrations in gray matter for 7-8 h postasphyxia, while lactate increased only briefly, suggesting decreased cerebral glucose utilization over this time. Although these data, as well as the concurrent suppression of breathing movements and electrocortical activity, support the concept of hypometabolic hypoperfusion, the significant increase of pyruvate and glycerol concentrations in dialysate fluid obtained from the cerebral cortex at 3-8 h after cord occlusion suggests an eventual loss of membrane integrity. The prolonged increase of breathing movements for many hours suggests loss of the pontine/thalamic control that produces the distinct pattern of fetal breathing movements.

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Section: Discussionmentioning

confidence: 74%

“…In the second group of fetuses, cerebral capillary blood flow was determined using permanently colored microspheres (22). A reference blood sample was withdrawn at a constant rate (0.8 ml/min) from the brachial artery catheter starting 1 min before and continuing until 3 min after the injection of each set of microspheres.…”

Section: Methodsmentioning

confidence: 99%

Changes in cerebral blood flow, cerebral metabolites, and breathing movements in the sheep fetus following asphyxia produced by occlusion of the umbilical cord

Yan¹,

Baburamani²,

Walker³

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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show abstract

“…48 In studies of cerebral metabolism and ECOG activity in fetal sheep subjected to UCOs, we have shown the ability to rapidly enact mechanisms to protect energy levels for membrane integrity by increasing cerebral blood flow, substrate extraction, and anaerobic metabolism and decreasing nonessential energy usage when oxygen availability is acutely limited. 49,50 Of note, the animals here studied also showed ECOG amplitude suppression during the UCOs with worsening acidosis indicating a decrease in synaptic energy use and with no difference in the timing for this between the UCO groups. 35 Accordingly, the near-term ovine fetal brain appears able to tolerate repetitive UCOs with severe acidemia and nadir pH *7.00 with no increase in overt necrotic cell injury, presumably through adaptive metabolic mechanisms such that the lower ischemic flow threshold of membrane failure with energy depletion was likely not reached.…”

Section: Discussionmentioning

confidence: 87%

Brain Injury and Inflammatory Response to Umbilical Cord Occlusions Is Limited With Worsening Acidosis in the Near-Term Ovine Fetus

Matushewski

Nygard

et al. 2016

Reprod. Sci.

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We hypothesized that repetitive umbilical cord occlusions (UCOs) with worsening fetal acidemia will lead to an inflammatory response within the brain and thereby brain injury which will be exacerbated by chronic hypoxemia and low-grade infection. Chronically instrumented fetal sheep served as controls (N = 10) or underwent repeated UCOs for up to 4 hours or until arterial pH was <7.00. Normoxic-UCO (N = 9) and hypoxic-UCO (N = 5) fetuses had arterial O2 saturation pre-UCOs of >55% and <55%, respectively, whereas lipopolysaccharide (LPS) UCO fetuses (N = 6) received LPS intra-amniotic (2 mg/h) starting 1 hour pre-UCOs. Animals were euthanized at 48 hours of recovery with fetal brains processed for assessment of inflammation (microglia and mast cell counts) and injury (necrosis-hematoxylin and eosin-and apoptosis-cleaved caspase-3 and terminal deoxynucleotidyl transferase dUTP nick end labeling [TUNEL]). Repetitive UCOs resulted in severe acidemia in most animals with pH approaching 7.00 for all 3 UCO groups. However, there was no significant effect on measures of brain inflammation or injury, except in the LPS-UCO animals where TUNEL-positive cells were increased in the hippocampus, although small animal numbers in the hypoxic-UCO group may have limited the ability to detect significance in their TUNEL cell findings. We were therefore unable to confirm our working hypothesis since the near-term ovine fetal brain showed remarkable tolerance for these cord occlusion insults and likely involving protective metabolic mechanisms, despite the severe acidemia noted.

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“…2 Consequently, such tests are popular and supported by national guidelines in many countries. [3][4][5] Lactate is a direct product of anaerobic glucose metabolism with animal studies demonstrating that levels rise earlier during hypoxia 6 and persist longer 7 than a low pH. While limited randomised trial data suggest scalp pH and lactate are equivalent in predicting neonatal compromise, [8][9][10] other data suggest prediction superiority for scalp lactate [11][12][13][14] and also cord lactate 15 over…”

Section: Introductionmentioning

confidence: 99%

Point‐of‐care measurement of fetal blood lactate – Time to trust a new device

Wang

Chua

Bouhadir

et al. 2017

Aust NZ J Obst Gynaeco

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Background: Point-of-care lactate devices are used worldwide for intrapartum decision making. Current practice is often based on Lactate Pro (Arkray) but its imminent product discontinuation necessitates determination of an optimal replacement device. Aims:To evaluate the performance of Lactate Pro and two other point-of-care devices, Lactate Pro 2 (Arkray) and StatStrip (Nova Biomedical), and to derive scalp lactate cut-offs equivalent to the current intervention trigger of >4.8 mmol/L. Materials and methods: Paired umbilical cord arterial and venous blood sam-ples from 109 births were tested on the three point-of-care products (two devices each), cross-compared with the reference method blood gas analyser.

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Cerebral blood flow and metabolism in relation to electrocortical activity with severe umbilical cord occlusion in the near-term ovine fetus

Cited by 45 publications

References 17 publications

Changes in cerebral blood flow, cerebral metabolites, and breathing movements in the sheep fetus following asphyxia produced by occlusion of the umbilical cord

Changes in cerebral blood flow, cerebral metabolites, and breathing movements in the sheep fetus following asphyxia produced by occlusion of the umbilical cord

Brain Injury and Inflammatory Response to Umbilical Cord Occlusions Is Limited With Worsening Acidosis in the Near-Term Ovine Fetus

Point‐of‐care measurement of fetal blood lactate – Time to trust a new device

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