Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
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J. Cereb. Blood Flow Metab. · May 2009
Deep hypothermia markedly activates the small ubiquitin-like modifier conjugation pathway; implications for the fate of cells exposed to transient deep hypothermic cardiopulmonary bypass.
Various cardiovascular operations are performed during conditions of deep hypothermic circulatory arrest. Here we investigated the effects of deep hypothermia on the small ubiquitin-like modifier (SUMO) conjugation pathway using a clinically relevant animal model of deep hypothermic cardiopulmonary bypass (DHCPB). ⋯ Activation of the SUMO conjugation pathway is believed to protect neurons from damage caused by low blood flow. This pathway may, therefore, play a key role in defining the outcome of cells exposed to DHCPB.
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J. Cereb. Blood Flow Metab. · Apr 2009
Cooling combined with immediate or delayed xenon inhalation provides equivalent long-term neuroprotection after neonatal hypoxia-ischemia.
Hypothermia (HT) improves outcome after neonatal hypoxia-ischemia. Combination therapy may extend neuroprotection. The noble anesthetic gas xenon (Xe) has an excellent safety profile. ⋯ One (immediate or with a delay) or 3 h Xe also significantly improved motor function (P=0.024). Females had significantly better motor scores than males, but no sex-dependent difference in pathology results. The neuroprotection of short, delayed Xe treatment would allow transport to specialist facilities to receive Xe.
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J. Cereb. Blood Flow Metab. · Apr 2009
Optimal location for arterial input function measurements near the middle cerebral artery in first-pass perfusion MRI.
One of the main difficulties in obtaining quantitative perfusion values from dynamic susceptibility contrast-magnetic resonance imaging is a correct arterial input function (AIF) measurement, as partial volume effects can lead to an erroneous shape and amplitude of the AIF. Cerebral blood flow and volume scale linearly with the area under the AIF, but shape changes of the AIF can lead to large, nonlinear errors. Current manual and automated AIF selection procedures do not guarantee the exclusion of partial volume effects from AIF measurements. ⋯ Three different sequences were investigated and evaluated on a voxel-by-voxel basis by comparison with the ground truth. Subsequently, the predictions were evaluated in an in vivo example. The findings are fourfold: AIF measurements should be performed in voxels completely outside the artery, here a linear relation should be assumed between DeltaR*2 and the concentration contrast agent, the exact optimal location differs per acquisition type, and voxels including a small MCA yield also correct AIF measurements for segmented echo planar imaging when a short echo time was used.
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J. Cereb. Blood Flow Metab. · Apr 2009
Time-course of cerebral perfusion and tissue oxygenation in the first 6 h after experimental subarachnoid hemorrhage in rats.
Present knowledge about hemodynamic and metabolic changes after subarachnoid hemorrhage (SAH) originates from neuromonitoring usually starting with aneurysm surgery and animal studies that have been focusing on the first 1 to 3 h after SAH. Most patients, however, are referred to treatment several hours after the insult. We examined the course of hemodynamic parameters, cerebral blood flow, and tissue oxygenation (ptiO2) in the first 6 h after experimental SAH. ⋯ Acute vasoconstriction after SAH is indicated by the marked discrepancy of cerebral perfusion pressure and local cortical blood flow. The excess tissue oxygenation several hours after SAH suggests disturbed oxygen utilization and cerebral metabolic depression. Aside from the sudden increase of intracranial pressure at the time of hemorrhage and delayed cerebral vasospasm, the occurrence of acute vasoconstriction and disturbed oxygen utilization may be additional factors contributing to secondary brain damage after SAH.
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J. Cereb. Blood Flow Metab. · Feb 2009
Estradiol after cardiac arrest and cardiopulmonary resuscitation is neuroprotective and mediated through estrogen receptor-beta.
We evaluated long-term administration of estrogen after cardiac arrest and cardiopulmonary resuscitation (CA/CPR) on neurohistopathological and behavioral outcome. We also examined the effect of estrogen receptor (ER) stimulation using ER-alpha agonist propyl pyrazole triol (PPT) and ER-beta agonist diarylpropionitrile (DPN) on neuronal survival after CA/CPR to determine whether possible neuroprotective effects of estrogen are ER-mediated. Male C57Bl/6 mice underwent 10 mins of CA/CPR and 3-day survival. ⋯ Estrogen receptor-beta agonist DPN reduced neuronal injury in the hippocampal CA1 field (29%+/-22% injured neurons) as compared with ER-alpha agonist PPT treatment (62%+/-33%; P<0.05). Injury was not different in hippocampal CA1 between vehicle and ER-alpha agonist-treated animals. We conclude that long-term E2 administration after CA/CPR is neuroprotective and that this effect is most likely mediated via ER-beta.