Search results for "Cortical Spreading Depression"
showing 6 items of 16 documents
Calcium and increase excitability promote tolerance against anoxia in hippocampal slices.
1999
We have previously demonstrated that anoxic preconditioning (APC) protects against a subsequent otherwise 'lethal' anoxic insult in hippocampal slices. Tested here are two hypotheses: (a) APC requires calcium to improve electrical recovery in hippocampal slices; and (b) mild excitation promotes preconditioning neuroprotection. Control hippocampal slices were given a single 'test' anoxic insult followed by reoxygenation. Experimental slices were preconditioned by three short anoxic insults of 1 min separated by 10 min of reoxygenation. At 30 min after the third 'conditioning' insult, slices underwent a 'test' anoxic insult [1 min of anoxic depolarization (AD)], and then slices were reoxygena…
Spontaneous Cortical Spreading Depression and Intracranial Pressure Following Acute Subdural Hematoma in a Rat
2012
Acute subdural hemorrhage (ASDH) is a frequent and devastating consequence of traumatic brain injury. Tissue damage develops rapidly and makes treatment even more difficult. Management of increased intracranial pressure (ICP) due to extravasated blood volume and brain swelling is often insufficient to control all adverse effects of ASDH. In addition to sheer volume, spontaneously triggered cortical spreading depression (CSD) that leads to cell death following ischemia or trauma may contribute to injury development after ASDH. Therefore, we explored the occurrence of CSD by tissue impedance (IMP) measurement in a rat model subjected to ASDH. IMP and intraventricular and mean arterial pressur…
Spreading Depression Induces Permanent Cell Swelling Under Penumbra Conditions
2000
Background. Spreading depression (SD) is known to go along with temporary breakdown of ion gradients and cell swelling which spontaneously normalizes. Here, the effects of SD at reduced flow conditions as encountered in the ischemic penumbra are examined.
Glutamate Enhances Brain Damage from Ischemia and Trauma
1997
The amino acid glutamate is a model agent to demonstrate the significance of neurotoxic mediator compounds in secondary brain damage from trauma, ischemia or other adverse conditions. Intensive research of the role of mediator compounds is clinically worthwile as more specific forms of treatment may emerge for the benefit of afflicted patients. In view of the great number of factors, cytokines, etc., which could play a role, it is mandatory that a mediator function in secondary brain damage is identified according to the stringent requirements established for that purpose. Glutamate has been shown — as is the case for only a few other agents — to meet all the criteria of a mediator of secon…
Temporal profile of gene induction after venous ischemia accompanied by spreading depression as compared to spreading depression alone
2002
Abstract The occlusion of two adjacent cortical veins is followed by a widespread reduction of rCBF and the occurrence of small infarcts, which become larger if spreading depression (SD) occurs. The model appears to be useful for studying penumbra pathophysiology. Here, the time course of gene expression in the penumbra was compared to those induced by the SD alone. In an experiment involving rats, an occlusion of two cortical veins was induced by i.v. rose bengal and fiberoptic illumination. Ten SDs were induced at 7-min intervals. Changes of the gene expression after 2, 8, 24 and 72 h were analysed for 13 genes by RT-PCR. The housekeeping gene glyceraldehyde-3-phosphate dehydrogenase (GAP…
Temporal Profile of Gene Induction After Venous Ischemia and Effects of Spreading Depression
2004
Occlusion of two adjacent cortical veins is followed by a widespread reduction of rCBF and the occurrence of small infarcts, which become larger if spreading depression (SD) occurs. The infarct matures over time with TUNEL-positive cells seen in the penumbra up to 4 days after vein occlusion. Caspase inhibition with zVAD.fmk reduces infarct size. Here, the time course of gene expression in the penumbra is compared to that induced by SD alone.