Structural remodeling of gray matter astrocytes in the neonatal pig brain after hypoxia/ischemia

Glia ◽  
2009 ◽  
Vol 58 (2) ◽  
pp. 181-194 ◽  
Author(s):  
Susan M. Sullivan ◽  
S. Tracey Björkman ◽  
Stephanie M. Miller ◽  
Paul B. Colditz ◽  
David V. Pow
Keyword(s):  
Gray Matter ◽  
Structural Remodeling ◽  
Pig Brain ◽  
Hypoxia Ischemia ◽  
Neonatal Pig

Liver Enzymes Cannot Be Used to Predict Liver Damage after Global Hypoxia-Ischemia in a Neonatal Pig Model

Neonatology ◽  
2009 ◽  
Vol 96 (4) ◽  
pp. 211-218 ◽  
Author(s):  
Mathias Karlsson ◽  
Saulius Satas ◽  
Janet Stone ◽  
Helen Porter ◽  
Marianne Thoresen
Keyword(s):  
Liver Damage ◽  
Liver Enzymes ◽  
Pig Model ◽  
Hypoxia Ischemia ◽  
Neonatal Pig

Neonatal pig brain: lack of heating during Doppler US.

Radiology ◽  
1998 ◽  
Vol 207 (2) ◽  
pp. 525-528 ◽  
Author(s):  
G A Taylor ◽  
C E Barnewolt ◽  
P S Dunning
Keyword(s):  
Doppler Us ◽  
Pig Brain ◽  
Neonatal Pig

scholarly journals Use of Mitochondrial Inhibitors to Demonstrate That Cytochrome Oxidase Near-Infrared Spectroscopy Can Measure Mitochondrial Dysfunction Noninvasively in the Brain

1999 ◽  
Vol 19 (1) ◽  
pp. 27-38 ◽  
Author(s):  
Chris E. Cooper ◽  
Mark Cope ◽  
Roger Springett ◽  
Philip N. Amess ◽  
Juliet Penrice ◽  
...  
Keyword(s):  
Infrared Spectroscopy ◽  
Cytochrome Oxidase ◽  
Near Infrared Spectroscopy ◽  
Redox State ◽  
Near Infrared ◽  
Blood Oxygenation ◽  
Concentration Addition ◽  
Pig Brain ◽  
Infrared Measurements ◽  
Neonatal Pig

The use of near-infrared spectroscopy to measure noninvasively changes in the redox state of cerebral cytochrome oxidase in vivo is controversial. We therefore tested these measurements using a multiwavelength detector in the neonatal pig brain. Exchange transfusion with perfluorocarbons revealed that the spectrum of cytochrome oxidase in the near-infrared was identical in the neonatal pig, the adult rat, and in the purified enzyme. Under normoxic conditions, the neonatal pig brain contained 15 μmol/L deoxyhemoglobin, 29 μmol/L oxyhemoglobin, and 1.2 μmol/L oxidized cytochrome oxidase. The mitochondrial inhibitor cyanide was used to determine whether redox changes in cytochrome oxidase could be detected in the presence of the larger cerebral hemoglobin concentration. Addition of cyanide induced full reduction of cytochrome oxidase in both blooded and bloodless animals. In the blooded animals, subsequent anoxia caused large changes in hemoglobin oxygenation and concentration but did not affect the cytochrome oxidase near-infrared signal. Simultaneous blood oxygenation level-dependent magnetic resonance imaging measurements showed a good correlation with near-infrared measurements of deoxyhemoglobin concentration. Possible interference in the near-infrared measurements from light scattering changes was discounted by simultaneous measurements of the optical pathlength using the cerebral water absorbance as a standard chromophore. We conclude that, under these conditions, near-infrared spectroscopy can accurately measure changes in the cerebral cytochrome oxidase redox state.

Biopterin in the acute phase of hypoxia–ischemia in a neonatal pig model

2008 ◽  
Vol 30 (1) ◽  
pp. 1-6 ◽  
Author(s):  
Hiroki Fujioka ◽  
Haruo Shintaku ◽  
Hidehiko Nakanishi ◽  
Tae-Jang Kim ◽  
Satoshi Kusuda ◽  
...  
Keyword(s):  
Acute Phase ◽  
Pig Model ◽  
Hypoxia Ischemia ◽  
Neonatal Pig

Real-time Monitoring of Hemodynamic Changes in Neonatal Pig Brain with Head Trauma Injury

2006 ◽  
Author(s):  
Chao Zhou ◽  
Turgut Durduran ◽  
Guoqiang Yu ◽  
Stephanie Eucker ◽  
Stuart Friess ◽  
...  
Keyword(s):  
Real Time ◽  
Head Trauma ◽  
Real Time Monitoring ◽  
Hemodynamic Changes ◽  
Pig Brain ◽  
Neonatal Pig ◽  
Trauma Injury

Melatonin receptors in neonatal pig brain and pituitary gland

1999 ◽  
Vol 26 (1) ◽  
pp. 43-49 ◽  
Author(s):  
L. M. Williams ◽  
L. T. Hannah ◽  
J. M. Bassett
Keyword(s):  
Pituitary Gland ◽  
Melatonin Receptors ◽  
Pig Brain ◽  
Neonatal Pig

scholarly journals Timing of Appearance of Late Oligodendrocyte Progenitors Coincides with Enhanced Susceptibility of Preterm Rabbit Cerebral White Matter to Hypoxia-Ischemia

2010 ◽  
Vol 30 (5) ◽  
pp. 1053-1065 ◽  
Author(s):  
Joshua R Buser ◽  
Kristen N Segovia ◽  
Justin M Dean ◽  
Kerst Nelson ◽  
Douglas Beardsley ◽  
...  
Keyword(s):  
White Matter ◽  
Gray Matter ◽  
Rabbit Model ◽  
White Matter Lesions ◽  
White Matter Injury ◽  
Microvascular Blood Flow ◽  
Cerebral White Matter ◽  
Caspase Activation ◽  
Oligodendrocyte Progenitors ◽  
Hypoxia Ischemia

Emerging evidence supports that premature infants are susceptible to both cerebral white and gray matter injury. In a fetal rabbit model of placental insufficiency, preterm rabbits at embryonic day 22 (E22) exhibited histologic evidence of gray matter injury but minimal white matter injury after global hypoxia-ischemia (H-I). We hypothesized that the dissociation between susceptibility to gray and white matter injury at E22 was related to the timing of appearance of late oligodendrocyte progenitors (preOLs) that are particularly vulnerable in preterm human white matter lesions. During normal rabbit oligodendrocyte (OL) lineage progression, early OL progenitors predominated at E22. PreOL density increased between E24 and E25 in major forebrain white matter tracts. After H-I at E22 and E25, we observed a similar magnitude of cerebral H-I, assessed by cortical microvascular blood flow, and gray matter injury, assessed by caspase activation. However, the increased preOL density at E25 was accompanied by a significant increase in acute white matter injury after H-I that coincided with enhanced preOL degeneration. At E29, significant white matter atrophy developed after H-I at E25 but not E22. Thus, the timing of appearance of preOLs coincided with onset of a developmental window of enhanced white but not gray matter susceptibility to H-I.

scholarly journals Neither Xenon nor Fentanyl Induces Neuroapoptosis in the Newborn Pig Brain

2013 ◽  
Vol 119 (2) ◽  
pp. 345-357 ◽  
Author(s):  
Hemmen Sabir ◽  
Sarah Bishop ◽  
Nicki Cohen ◽  
Elke Maes ◽  
Xun Liu ◽  
...  
Keyword(s):  
Apoptotic Cell ◽  
Fold Increase ◽  
Brain Regions ◽  
Cell Counting ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Inhalation Anesthetics ◽  
Ischemic Brain ◽  
Neonatal Pigs ◽  
Pig Brain ◽  
Neonatal Pig

Abstract Background: Some inhalation anesthetics increase apoptotic cell death in the developing brain. Xenon, an inhalation anesthetic, increases neuroprotection when combined with therapeutic hypothermia after hypoxic-ischemic brain injury in newborn animals. The authors, therefore, examined whether there was any neuroapoptotic effect of breathing 50% xenon with continuous fentanyl sedation for 24 h at normothermia or hypothermia on newborn pigs. Methods: Twenty-six healthy pigs (<24-h old) were randomized into four groups: (1) 24 h of 50% inhaled xenon with fentanyl at hypothermia (Trec = 33.5°C), (2) 24 h of 50% inhaled xenon with fentanyl at normothermia (Trec = 38.5°C), (3) 24 h of fentanyl at normothermia, or (4) nonventilated juvenile controls at normothermia. Five additional nonrandomized pigs inhaled 2% isoflurane at normothermia for 24 h to verify any proapoptotic effect of inhalation anesthetics in our model. Pathological cells were morphologically assessed in cortex, putamen, hippocampus, thalamus, and white matter. To quantify the findings, immunostained cells (caspase-3 and terminal deoxynucleotidyl transferase–mediated deoxyuridine-triphosphate nick-end labeling) were counted in the same brain regions. Results: For groups (1) to (4), the total number of apoptotic cells was less than 5 per brain region, representing normal developmental neuroapoptosis. After immunostaining and cell counting, regression analysis showed that neither 50% xenon with fentanyl nor fentanyl alone increased neuroapoptosis. Isoflurane caused on average a 5- to 10-fold increase of immunostained cells. Conclusion: At normothermia or hypothermia, neither 24 h of inhaled 50% xenon with fentanyl sedation nor fentanyl alone induces neuroapoptosis in the neonatal pig brain. Breathing 2% isoflurane increases neuroapoptosis in neonatal pigs.

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