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. · Sep 2009
Neurogenesis and angiogenesis within the ipsilateral thalamus with secondary damage after focal cortical infarction in hypertensive rats.
Neurogenesis and angiogenesis in the subventricular zone and peri-infarct region have been confirmed. However, newly formed neuronal cells and blood vessels that appear in the nonischemic ipsilateral ventroposterior nucleus (VPN) of the thalamus with secondary damage after stroke has not been previously studied. Twenty-four stroke-prone renovascular hypertensive rats were subjected to distal right middle cerebral artery occlusion (MCAO) or sham operation. 5'-Bromo-2'-deoxyuridine (BrdU) was used to label cell proliferation. ⋯ Moreover, BrdU(+)/nestin(+) cells and BrdU(+)/NeuN(+) cells were detected at day 14 after MCAO. In addition, the ischemic rats showed a significant increase in vascular density in the ipsilateral VPN compared with the sham-operated rats. These results suggest that secondary damage with neurogenesis and angiogenesis of the ipsilateral VPN of the thalamus occurs after focal cortical infarction.
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J. Cereb. Blood Flow Metab. · Aug 2009
Randomized Controlled TrialBiologic effects of simvastatin in patients with aneurysmal subarachnoid hemorrhage: a double-blind, placebo-controlled randomized trial.
Recently, two randomized controlled phase II studies showed that acute initiation of statin treatment directly after aneurysmal subarachnoid hemorrhage (SAH) decreases the incidence of radiologic vasospasm and clinical signs of delayed cerebral ischemia (DCI), and even reduces mortality. It was hypothesized that the beneficial effect resulted from pleiotropic effects of statins. The purpose of this study was to investigate the biologic effects of acute statin treatment in patients with SAH. ⋯ With regard to primary outcomes, there were significant differences by treatment group for total cholesterol and low-density lipoprotein (LDL) cholesterol (P<0.0001), but not for parameters of coagulation, fibrinolysis, endothelium function, and inflammation. With regard to secondary outcomes, no differences were observed in the incidence of transcranial Doppler vasospasm, clinical signs of DCI, and poor outcome. We conclude that both the primary and secondary outcome results of this study do not support a beneficial effect of simvastatin in patients with SAH.
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J. Cereb. Blood Flow Metab. · Aug 2009
Substance P is associated with the development of brain edema and functional deficits after traumatic brain injury.
Brain edema and swelling is a critical factor in the high mortality and morbidity associated with traumatic brain injury (TBI). Despite this, the mechanisms associated with its development are poorly understood and interventions have not changed in over 30 years. Although neuropeptides and neurogenic inflammation have been implicated in peripheral edema formation, their role in the development of central nervous system edema after brain trauma has not been investigated. ⋯ Inhibition of SP action by administration of the neurokinin-1 (NK1) antagonist, N-acetyl-L-tryptophan, at 30 mins after trauma attenuated vascular permeability and edema formation. Administration of the NK1 antagonist also improved both motor and cognitive neurologic outcomes. These findings suggest that SP release is integrally linked to the increased vascular permeability and edema formation after brain trauma, and that treatment with an NK1 receptor antagonist reduces edema and improves neurologic outcome.
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J. Cereb. Blood Flow Metab. · Jun 2009
A phase-contrast MRI study of physiologic cerebral venous flow.
Although crucial in regulating intracranial hydrodynamics, the cerebral venous system has been rarely studied because of its structural complexity and individual variations. The purpose of our study was to evaluate the organization of cerebral venous system in healthy adults. Phase-contrast magnetic resonance imaging (PC-MRI) was performed in 18 healthy volunteers, in the supine position. ⋯ Cerebrospinal fluid aqueductal and cervical stroke volumes were 41+/-22 and 460+/-149 microL, respectively. Our results emphasize the variability of venous drainage for side dominance and jugular/epidural organization. The pulsatility of venous outflow and the role it plays in the regulation of intracranial pressure require further investigation.
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J. Cereb. Blood Flow Metab. · Jun 2009
Neuroinflammation extends brain tissue at risk to vital peri-infarct tissue: a double tracer [11C]PK11195- and [18F]FDG-PET study.
Focal cerebral ischemia elicits strong inflammatory responses involving activation of resident microglia and recruitment of monocytes/macrophages. These cells express peripheral benzodiazepine receptors (PBRs) and can be visualized by positron emission tomography (PET) using [(11)C]PK11195 that selectively binds to PBRs. Earlier research suggests that transient ischemia in rats induces increased [(11)C]PK11195 binding within the infarct core. ⋯ Contrasting with earlier data for transient ischemia, no [(11)C]PK11195 binding was found in the infarct core. Rather, permanent ischemia caused increased [(11)C]PK11195 binding in the normoperfused peri-infarct zone (mean standard uptake value (SUV): 1.93+/-0.49), colocalizing with a 60% increase in the [(18)F]FDG metabolic rate constant with accumulated activated microglia and macrophages. These results suggest that after permanent focal ischemia, neuroinflammation occurring in the normoperfused peri-infarct zone goes along with increased energy demand, therefore extending the tissue at risk to areas adjacent to the infarct.