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. · Jan 2009
Magnetic resonance imaging assessment of regional cerebral blood flow after asphyxial cardiac arrest in immature rats.
Cerebral blood flow (CBF) alterations after asphyxial cardiac arrest (CA) are not defined in developmental animal models or humans. We characterized regional and temporal changes in CBF from 5 to 150 mins after asphyxial CA of increasing duration (8.5, 9, 12 min) in postnatal day (PND) 17 rats using the noninvasive method of arterial spin-labeled magnetic resonance imaging (ASL-MRI). We also assessed blood-brain barrier (BBB) permeability, and evaluated the relationship between CBF and mean arterial pressure after resuscitation. ⋯ BBB was impermeable to gadoteridol 150 mins after CA. CBF in the 12-min CA group was blood pressure passive at 60 min assessed via infusion of epinephrine. ASL-MRI assessment of CBF after asphyxial CA in PND 17 rats reveals marked duration and region-specific reperfusion patterns and identifies possible new therapeutic targets.
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J. Cereb. Blood Flow Metab. · Jan 2009
Cytosolic Ca2+ oscillations in human cerebrovascular endothelial cells after subarachnoid hemorrhage.
Molecular mechanisms of cerebral vasospasm after subarachnoid hemorrhage (SAH) include specific modes of cell signaling like activation of nuclear factor (NF)-kappaB and vascular cell adhesion molecules (VCAM)-1 expression. The study's hypothesis is that cisternal cerebral spinal fluid (CSF) from patients after SAH may cause Ca(2+) oscillations which induce these modes of vascular inflammation in an in vitro model of human cerebral endothelial cells (HCECs). HCECs were incubated with cisternal CSF from 10 SAH patients with confirmed cerebral vasospasm. ⋯ In analogy to the reduction of Ca(2+) oscillation frequency, the blockers impaired HCEC contraction, NF-kappaB activation, and VCAM-1 expression. Cisternal SAH-CSF induces cytosolic Ca(2+) oscillations in HCEC that results in cellular constriction, NF-kappaB activation, and VCAM-1 expression. The Ca(2+) oscillations depend on the function of ER Ca(2+)-ATPase and IP3-sensitive Ca(2+) channels.