Prominent white matter lesions develop in Mongolian gerbils treated with 100% normobaric oxygen after global brain ischemia

Mickel, Hubert S.; Kempski, Oliver; Feuerstein, Giora; Parisi, Joseph E.; Webster, Henry deF.

doi:10.1007/bf00296104

Cited by 29 publications

(14 citation statements)

References 24 publications

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“…Gerbils subjected to 15 min of bilateral carotid artery ligation and then given 100% O2 for 3 h showed a higher mortality than those breathing room air (23). Neuropathologic examination revealed an increased myelin damage in the oxygen-treated animals (24). Neurons, however, appeared better preserved when given oxygen.…”

Section: Morphologic Examinationmentioning

confidence: 90%

Hypoxemia and Reoxygenation with 21% or 100% Oxygen in Newborn Pigs: Changes in Blood Pressure, Base Deficit, and Hypoxanthine and Brain Morphology

et al. 1992

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ABSTRACT. To study whether room air is as effective as 100% 0 2 in resuscitation after hypoxia, hypoxemia (Pao2 2.3-4.3 kPa) was induced in newborn pigs (2-5 d old) by ventilation with 8% O2 in nitrogen. When systolic blood pressure had fallen to 20 mm Hg, animals were randomly reoxygenated with either 21% Oz (group 1, n = 9) or 100% 0 2 (group 2, n = 11) for 20 min followed by 21% O2 in both groups. Controls (group 3, n = 5) were ventilated with 21% 0 2 throughout the experiment. Base deficit peaked at 31 f 5 mmol/L (mean f SD) for both hypoxic groups at 5 min of reoxygenation and then normalized over the following 3 h. There were no statistically significant differences between the two groups during reoxygenation concerning blood pressure, heart rate, base deficit, or plasma hypoxanthine. Hypoxanthine peaked at 165 +. 40 and 143 +. 42 ~m o l / L in group 1 and 2 (NS), respectively, and was eliminated monoexponentially in both groups with an initial half-life for excess hypoxanthine of 48 f 21 and 51 +. 27 min (NS), respectively. Blinded pathologic examination of cerebral cortex, cerebellum, and hippocampus after 4 d showed no statistically significant differences with regard to brain damage. We conclude that 21% 0 2 is as effective as 100% O2 for normalizing blood pressure, heart rate, base deficit, and plasma hypoxanthine after severe neonatal hypoxemia in piglets and that the extent of the hypoxic brain damage is similar in the two groups. (Pediatr Res 32: 107-113,1992)

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Section: Morphologic Examinationmentioning

confidence: 90%

Hypoxemia and Reoxygenation with 21% or 100% Oxygen in Newborn Pigs: Changes in Blood Pressure, Base Deficit, and Hypoxanthine and Brain Morphology

et al. 1992

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“…In contrast to the concept that provision of high oxygen after global ischemia should promote aerobic energy metabolism, hyperoxic reperfusion elevates brain lactate, impairs metabolism of glucose to aerobic energy metabolites, and worsens the post-ischemic oxidized shift in tissue redox state (Feng et al, 1998;Liu et al, 1998;Mickel et al, 1987;Richards et al, 2007). Hyperoxic resuscitation also promotes damage to white matter in gerbils (Mickel et al, 1990), and hippocampal neuronal death in dogs (Balan et al, 2006;Vereczki et al, 2006). On a neurological level, hyperoxia increases 14-day mortality in gerbils (Mickel et al, 1987), and worsens 12-to 24-h neurological outcome in dogs (Balan et al, 2006;Vereczki et al, 2006;Zwemer et al, 1994).…”

mentioning

confidence: 96%

“…Nevertheless, considering the failure of numerous interventions in clinical trials for ischemic brain injury that were proven effective in animal models (Liebeskind et al, 2001), caution should be taken when interpreting the animal data. While normoxia appeared to reduce white matter damage in gerbils at 14 days of reperfusion, this finding was not quantified (Mickel et al, 1990). A highly quantitative and non-biased stereologic approach was used to demonstrate reduced hippocampal neuronal death in the clinically more relevant canine cardiac arrest model (Balan et al, 2006;Liu et al, 1998;Vereczki et al, 2006); however, these results were obtained at 24 h of reperfusion, while cell death continues for days to weeks following transient global cerebral ischemia.…”

mentioning

confidence: 99%

Hyperoxic Reperfusion after Global Cerebral Ischemia Promotes Inflammation and Long-Term Hippocampal Neuronal Death

Hazelton

Balan

Elmer

et al. 2010

Journal of Neurotrauma

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In this study we tested the hypothesis that long-term neuropathological outcome is worsened by hyperoxic compared to normoxic reperfusion in a rat global cerebral ischemia model. Adult male rats were anesthetized and subjected to bilateral carotid arterial occlusion plus bleeding hypotension for 10 min. The rats were randomized to one of four protocols: ischemia=normoxia (21% oxygen for 1 h), ischemia=hyperoxia (100% oxygen for 1 h), sham=normoxia, and sham=hyperoxia. Hippocampal CA1 neuronal survival and activation of microglia and astrocytes were measured in the hippocampi of the animals at 7 and 30 days post-ischemia. Morris water maze testing of memory was performed on days 23-30. Compared to normoxic reperfusion, hyperoxic ventilation resulted in a significant decrease in normal-appearing neurons at 7 and 30 days, and increased activation of microglia and astrocytes at 7, but not at 30, days of reperfusion. Behavioral deficits were also observed following hyperoxic, but not normoxic, reperfusion. We conclude that early post-ischemic hyperoxic reperfusion is followed by greater hippocampal neuronal death and cellular inflammatory reactions compared to normoxic reperfusion. The results of these long-term outcome studies, taken together with previously published results from short-term experiments performed with large animals, support the hypothesis that neurological outcome can be improved by avoiding hyperoxic resuscitation after global cerebral ischemia such as that which accompanies cardiac arrest.

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“…Elevated levels of free oxygen radicals can cause loss of neurons and induce neurological deficits (Balentine, 1966;Mickel et al, 1990;Nakashima et al, 1999;Oh and Betz, 1991). In an experimental Under normal atmospheric conditions oxygen is mainly bound to hemoglobin.…”

Section: Side Effects Of Hyperoxic Treatmentmentioning

confidence: 99%

Brain Tissue Oxygen Monitoring and Hyperoxic Treatment in Patients with Traumatic Brain Injury

Beynon

Kiening

Orakcioglu

et al. 2012

Journal of Neurotrauma

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Cerebral ischemia is a well-recognized contributor to high morbidity and mortality after traumatic brain injury (TBI). Standard of care treatment aims to maintain a sufficient oxygen supply to the brain by avoiding increased intracranial pressure (ICP) and ensuring a sufficient cerebral perfusion pressure (CPP). Devices allowing direct assessment of brain tissue oxygenation have showed promising results in clinical studies, and their use was implemented in the Brain Trauma Foundation Guidelines for the treatment of TBI patients in 2007. Results of several studies suggest that a brain tissue oxygen-directed therapy guided by these monitors may contribute to reduced mortality and improved outcome of TBI patients. Whether increasing the oxygen supply to supraphysiological levels has beneficial or detrimental effects on TBI patients has been a matter of debate for decades. The results of trials of hyperbaric oxygenation (HBO) have failed to show a benefit, but renewed interest in normobaric hyperoxia (NBO) in the treatment of TBI patients has emerged in recent years. With the increased availability of advanced neuromonitoring devices such as brain tissue oxygen monitors, it was shown that some patients might benefit from this therapeutic approach. In this article, we review the pathophysiological rationale and technical modalities of brain tissue oxygen monitors, as well as its use in studies of brain tissue oxygen-directed therapy. Furthermore, we analyze hyperoxia as a treatment option in TBI patients, summarize the results of clinical trials, and give insights into the recent findings of hyperoxic effects on cerebral metabolism after TBI.

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Prominent white matter lesions develop in Mongolian gerbils treated with 100% normobaric oxygen after global brain ischemia

Cited by 29 publications

References 24 publications

Hypoxemia and Reoxygenation with 21% or 100% Oxygen in Newborn Pigs: Changes in Blood Pressure, Base Deficit, and Hypoxanthine and Brain Morphology

Hypoxemia and Reoxygenation with 21% or 100% Oxygen in Newborn Pigs: Changes in Blood Pressure, Base Deficit, and Hypoxanthine and Brain Morphology

Hyperoxic Reperfusion after Global Cerebral Ischemia Promotes Inflammation and Long-Term Hippocampal Neuronal Death

Brain Tissue Oxygen Monitoring and Hyperoxic Treatment in Patients with Traumatic Brain Injury

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