Author pages are created from data sourced from our academic publisher partnerships and public sources.
Share This Author
Thresholds in cerebral ischemia - the ischemic penumbra.
Recent evidence indicates that immediate failure of basic functions such as synaptic transmission, ion pumping and energy metabolism in the ischemic brain, is critically dependent on residual blood flow, and that these functions fail at certain critical flow thresholds.
Pathophysiology and treatment of focal cerebral ischemia. Part I: Pathophysiology.
- B. Siesjö
- Biology, MedicineJournal of neurosurgery
The pathophysiology of lesions caused by focal cerebral ischemia, a complex interplay between loss of cellular calcium homeostasis and acidosis, plays an important role in the pathogenesis of ischemic cell damage.
Models for studying long‐term recovery following forebrain ischemia in the rat. 2. A 2‐vessel occlusion model
- Maj-lis Smith, G. Béndek, N. Dahlgren, I. Rosén, T. Wieloch, B. Siesjö
- MedicineActa neurologica Scandinavica
- 1 June 1984
By the use of intubation, muscle paralysis with suxamethonium chloride, and insertion of tail arterial and venous catheters, it was possible to induce reversible ischemia for long‐term recovery studies.
Neuroprotective Effects of a Novel Nitrone, NXY-059, after Transient Focal Cerebral Ischemia in the Rat
- S. Kuroda, R. Tsuchidate, M. L. Smith, K. R. Maples, B. Siesjö
- Medicine, BiologyJournal of cerebral blood flow and metabolism…
- 1 July 1999
Studies of the transfer constant of [14C]NXY-059 showed that, in contrast to PBN, this more soluble nitrone penetrates the blood-brain barrier less extensively, suggesting that the delayed events leading to infarction may be influenced by reactions occurring at the blood–endothelial interface.
Calcium in ischemic cell death.
Calcium is one of the triggers involved in ischemic cell death, whatever the mechanism, and has been demonstrated among glutamate release, calcium influx, and enhanced production of reactive metabolites such as .O2-, .OH, and nitric oxide.
The density and distribution of ischemic brain injury in the rat following 2–10 min of forebrain ischemia
Mild brain damage was observed in some animals already after 2 min, and more consistently after 4 min of ischemia, and selective neuronal necrosis of the cerebral cortex worsened into infarction after higher doses of insult.
Regulation of Brain-Derived Neurotrophic Factor Gene Expression after Transient Middle Cerebral Artery Occlusion with and without Brain Damage
The observed pattern of gene expression after MCAO agrees well with a neuroprotective role of BDNF in cortical neurons, and elevated levels of NGF and BDNF protein could also increase synaptic efficacy in the postischemic phase, which may promote epileptogenesis.
Ischemic penumbra in a model of reversible middle cerebral artery occlusion in the rat
Flow distribution in a rat model of reversible middle cerebral artery (MCA) occlusion is defined to allow delineation of the metabolic aberrations responsible for the subsequent infarction to help define large parts of the neocortex as perifocal areas which lend themselves to studies of metabolic events leading to infarctions.
Brain Cortical Fatty Acids and Phospholipids During and Following Complete and Severe Incomplete Ischemia
The present in vivo results fail to support the hypothesis that peroxidation of membrane lipids is of primary importance for ischemic brain cell damage.