Journal of neurosurgical anesthesiology
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J Neurosurg Anesthesiol · Oct 2011
A novel technique for monitoring of fast variations in brain oxygen tension using an uncoated fluorescence quenching probe (Foxy AL-300).
A novel uncoated fluorescence quenching probe allows fast measurement of oxygen tension in vessels and tissue. The present study reports the first use of the technology for dual measurements of arterial (paO(2)) and brain tissue oxygen tension (ptiO(2)) during hypoxic challenge in a pig model. ⋯ The present study demonstrates the feasibility of pO(2) measurements in macrocirculation and cerebral microcirculation using a novel uncoated fluorescence quenching probe. The technology allows for real-time investigation of pO(2) changes at a temporal resolution of 0.05 to 10 Hz.
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J Neurosurg Anesthesiol · Oct 2011
Isoflurane preconditioning protects astrocytes from oxygen and glucose deprivation independent of innate cell sex.
Isoflurane exposure can protect the mammalian brain from subsequent insults such as ischemic stroke. However, this protective preconditioning effect is sexually dimorphic, with isoflurane preconditioning decreasing male while exacerbating female brain damage in a mouse model of cerebral ischemia. Emerging evidence suggests that innate cell sex is an important factor in cell death, with brain cells having sex-specific sensitivities to different insults. We used an in vitro model of isoflurane preconditioning and ischemia to test the hypothesis that isoflurane preconditioning protects male astrocytes while having no effect or even a deleterious effect in female astrocytes after subsequent oxygen and glucose deprivation (OGD). ⋯ More studies are needed to determine how cell type and cell sex may impact on anesthetic preconditioning and subsequent ischemic outcomes in the brain.
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J Neurosurg Anesthesiol · Oct 2011
The effects of insulin, glucagon, glutamate, and glucose infusion on blood glutamate and plasma glucose levels in naive rats.
Elevated levels of glutamate in brain fluids, in the context of several neurodegenerative conditions, are associated with a worsened neurological outcome. Because there is a clear relationship between brain glutamate levels and glutamate levels in the blood, and an association of the latter with stress, the purpose of this study was to investigate the effects of glucose, insulin, and glucagon on rat blood glutamate levels. ⋯ The results of this study demonstrate that glucose, insulin, and glucagon significantly reduce blood glutamate levels. The effect of insulin is immediate and transient, whereas the effect of glucagon is delayed but longer lasting, suggesting that the sensitivity of pancreatic glucagon and insulin-secreting cells to glutamate is dependent on glucose concentration. The results of this study provide insight into blood glutamate homeostasis and may assist in the implementation of new therapies for brain neuroprotection from excess glutamate.
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J Neurosurg Anesthesiol · Oct 2011
Intervertebral disc degeneration-induced expression of pain-related molecules: glial cell-derived neurotropic factor as a key factor.
Discogenic low back pain has been shown to develop into chronic intractable pain due to an unknown pathogenesis. To study the mechanism of discogenic pain, we analyzed the serial expression of pain-related molecules in the dorsal root ganglia (DRG) and thalamus using a newly developed rat model of disc degeneration. ⋯ The disc degeneration rat model described herein led to significant pain of a chronic nature. The gradual and persistent increase of GDNF in both the thalamus and DRG suggests that GDNF might be a key factor in the development of intractable, chronic discogenic pain.