Acute neuronal injury after hypoxia is influenced by the reoxygenation mode in juvenile hippocampal slice cultures

Graulich, Johannes; Hoffmann, Ulrich; Maier, Rolf F.; Ruscher, Karsten; Pomper, Jörn K.; Ko, Hae-Kyung; Gabriel, Siegrun; Obladen, Michael; Heinemann, Uwe

doi:10.1016/s0165-3806(02)00365-6

Cited by 21 publications

(14 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In cultured hippocampal slices at least 30-min OGD has been previously applied to induce ischemic neuronal death [8,14,15], and up to an hour and more [16,17,18,19,20]. Such long-term OGD is known to cause significant neuronal damage.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Morphological and functional changes in rat hippocampal slice cultures after short‐term oxygen‐glucose deprivation

Lushnikova

Воронин

Malyarevskyy

et al. 2004

J Cellular Molecular Medi

View full text Add to dashboard Cite

To study effects of short‐term cerebral ischemia, hippocampal slice cultures were subjected to oxygen and glucose deprivation (OGD) followed by a period of normoxic reoxygenation. Propidium iodide staining, and MTT/formazanassay were used to evaluate cell viability and metabolic activity. CA1 pyramidal cells were analyzed at the light‐and electron microscopic levels. Cell damage was found to be insignificant during the first hour after 10 min OGD but profound following 4 h, showing delayed neuronal cell damage caused by short‐term OGD. Our model can be used to characterize the mechanisms of cell damage caused by mild cerebral ischemia. These data might apply to further development of neuroprotective tools for the treatment of brain diseases.

show abstract

Section: Discussionmentioning

confidence: 99%

“…Further, short-term episodes of OGD in cultured hippocampal slices are considered to be protective against the following prolonged anoxia [24,25], and called "ischemic preconditioning". It should be also noted that at least two factors, deprivation and reoxygenation, may cause the tissue response [18,26,27].…”

Section: Discussionmentioning

confidence: 99%

Morphological and functional changes in rat hippocampal slice cultures after short‐term oxygen‐glucose deprivation

Lushnikova

Воронин

Malyarevskyy

et al. 2004

J Cellular Molecular Medi

View full text Add to dashboard Cite

show abstract

“…Cell death was determined 24 hours after OGD by measuring the release of LDH into the medium, using a colorimetric assay (Cytotoxicity Detection Kit; Roche Diagnostics) according to the manufacturer's instructions. To evaluate the damaged region within the slice, cultures were labeled with propidium iodide, the staining for which correlates with LDH release in models of excitotoxicity (75) and hypoxia (76). Briefly, after collecting media for the LDH assay, slices were incubated in propidium iodide-containing medium (10 μM) for 1 hour at 37°C.…”

Section: Methodsmentioning

confidence: 99%

Extrasynaptic glutamate release through cystine/glutamate antiporter contributes to ischemic damage

Soria¹,

Pérez-Samartı́n²,

Martín³

et al. 2014

J. Clin. Invest.

105

112

View full text Add to dashboard Cite

“…Previous recommendations were to be generous with oxygen, but recent guidelines from a number of countries, e.g. Australia, Canada, Finland, the Netherlands, Sweden, and the United Kingdom recommend initial ventilation with air, because of the results from several experimental (2)(3)(4)(5) and clinical (6 -13) studies indicating that resuscitation with 100% oxygen is harmful. In the clinical studies, the time of exposure to 100% oxygen was typically 5-7 min (8,13), whereas only one animal study (5) has investigated an exposure time to oxygen less than 15 min.…”

mentioning

confidence: 99%

High Brain Tissue Oxygen Tension During Ventilation With 100% Oxygen After Fetal Asphyxia in Newborn Sheep

et al. 2009

View full text Add to dashboard Cite

ABSTRACT:The optimal inhaled oxygen fraction for newborn resuscitation is still not settled. We hypothesized that short-lasting oxygen ventilation after intrauterine asphyxia would not cause arterial or cerebral hyperoxia, and therefore be innocuous. The umbilical cord of fetal sheep was clamped and 10 min later, after delivery, ventilation with air (n ϭ 7) or with 100% oxygen for 3 (n ϭ 6) or 30 min (n ϭ 5), followed by air, was started. Among the 11 lambs given 100% oxygen, oxygen tension (P O2 ) was 10.7 (1.8 -56) kPa [median (range)] in arterial samples taken after 2.5 min of ventilation. In those ventilated with 100% oxygen for 30 min, brain tissue P O2 (Pbt O2 ) increased from less than 0.1 kPa in each lamb to individual maxima of 56 (30 -61) kPa, whereas in those given oxygen for just 3 min, Pbt O2 peaked at 4.2 (2.9 -46) kPa. The maximal Pbt O2 in airventilated lambs was 2.9 (0.8 -5.4) kPa. Heart rate and blood pressure increased equally fast in the three groups. Thus, prolonged ventilation with 100% oxygen caused an increase in Pbt O2 of a magnitude previously only reported under hyperbaric conditions. Reducing the time of 100% oxygen ventilation to 3 min did not consistently avert systemic hyperoxia. (Pediatr Res 65: 57-61, 2009) C urrent guidelines from the International Liaison Committee on Resuscitation breathe considerable uncertainty as to how much supplementary oxygen should be given during resuscitation of newborn asphyxiated infants (1). Previous recommendations were to be generous with oxygen, but recent guidelines from a number of countries, e.g. Australia, Canada, Finland, the Netherlands, Sweden, and the United Kingdom recommend initial ventilation with air, because of the results from several experimental (2-5) and clinical (6 -13) studies indicating that resuscitation with 100% oxygen is harmful. In the clinical studies, the time of exposure to 100% oxygen was typically 5-7 min (8,13), whereas only one animal study (5) has investigated an exposure time to oxygen less than 15 min.We speculated that very short times of exposure might not allow systemic hyperoxia to develop and so be harmless to the newborn infant, except for a possible negative effect on the lungs. In fact, the pulse oximetric saturation at 3 min after birth is usually below 80% (14,15) in the normal air-breathing infant, suggesting the presence of cardiac or pulmonary rightto-left shunts. One might expect that such shunts would delay the appearance of arterial hyperoxemia in the infant breathing pure oxygen. However, this has been studied neither in normal nor in asphyxiated subjects.We used a sheep model of term intrauterine asphyxia with postnatal resuscitation, and hypothesized that hyperoxia of arterial blood and of brain tissue could be prevented by limiting the period of ventilation with 100% oxygen to 3 min. We also investigated whether the speed of circulatory recovery, as reflected by the heart rate (HR) and mean arterial blood pressure (MAP) responses, and the speed of recovery of brain oxygenation, as reflected ...

show abstract

Acute neuronal injury after hypoxia is influenced by the reoxygenation mode in juvenile hippocampal slice cultures

Cited by 21 publications

References 37 publications

Morphological and functional changes in rat hippocampal slice cultures after short‐term oxygen‐glucose deprivation

Morphological and functional changes in rat hippocampal slice cultures after short‐term oxygen‐glucose deprivation

Extrasynaptic glutamate release through cystine/glutamate antiporter contributes to ischemic damage

High Brain Tissue Oxygen Tension During Ventilation With 100% Oxygen After Fetal Asphyxia in Newborn Sheep

Contact Info

Product

Resources

About