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
Comparative StudyCritical closing pressure: comparison of three methods.
Critical closing pressure (CCP) is an arterial pressure threshold below which small arterial vessels collapse. Our aim was to compare different methods to estimate CCP in the cerebrovascular circulation using the relationships between transcranial Doppler flow velocity (FV), laser-Doppler flux (LDF), and arterial blood pressure (ABP). A total of 116 experiments in rabbits were analyzed retrospectively. ⋯ Critical closing pressures obtained from FV waveform and CA correlated with mean ICP before CA (R=0.40; P=0.001). In conclusion strong correlation exists between CCP values obtained by means of FV and LDF during cardiac arrest. However, predictions of CCP using TCD waveform analysis show substantial differences from values of CCP recorded during cardiac arrest.
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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
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. · 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. · Feb 2009
Glibenclamide reduces inflammation, vasogenic edema, and caspase-3 activation after subarachnoid hemorrhage.
Subarachnoid hemorrhage (SAH) causes secondary brain injury due to vasospasm and inflammation. Here, we studied a rat model of mild-to-moderate SAH intended to minimize ischemia/hypoxia to examine the role of sulfonylurea receptor 1 (SUR1) in the inflammatory response induced by SAH. mRNA for Abcc8, which encodes SUR1, and SUR1 protein were abundantly upregulated in cortex adjacent to SAH, where tumor-necrosis factor-alpha (TNFalpha) and nuclear factor (NF)kappaB signaling were prominent. In vitro experiments confirmed that Abcc8 transcription is stimulated by TNFalpha. ⋯ SAH caused a large increase in barrier permeability and disrupted the normal junctional localization of ZO-1, with glibenclamide significantly reducing both effects. In addition, SAH caused large increases in markers of inflammation, including TNFalpha and NFkappaB, and markers of cell injury or cell death, including IgG endocytosis and caspase-3 activation, with glibenclamide significantly reducing these effects. We conclude that block of SUR1 by glibenclamide may ameliorate several pathologic effects associated with inflammation that lead to cortical dysfunction after SAH.