Stroke; a journal of cerebral circulation
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Comparative Study
Superoxide generation links nociceptin/orphanin FQ (NOC/oFQ) release to impaired N-methyl-D-aspartate cerebrovasodilation after brain injury.
Although activation of the N-methyl-D-aspartate (NMDA) receptor is thought to contribute to altered cerebrovascular regulation after traumatic brain injury, the effects of such injury on the vascular response to NMDA itself has been less well appreciated. The newly described opioid nociceptin/orphanin FQ (NOC/oFQ) elicits pial artery dilation, at least in part, in a prostaglandin-dependent manner and is released into cerebrospinal fluid after fluid percussion brain injury (FPI). Generation of superoxide anion (O(2)(-)) occurs after FPI, and a byproduct of cyclooxygenase metabolism is the generation of O(2)(-). This study was designed to determine whether NOC/oFQ generates O(2)(-), which in turn could link NOC/oFQ release to impaired NMDA-induced pial artery dilation after FPI. ⋯ These data show that NOC/oFQ, in concentrations present in cerebrospinal fluid after FPI, increased O(2)(-) production in a cyclooxygenase-dependent manner and contributes to such production after FPI. These data show that NOC/oFQ contributes to impaired NMDA-induced pial artery dilation after FPI. Therefore, these data suggest that cyclooxygenase-dependent O(2)(-) generation links NOC/oFQ release to impaired NMDA-induced cerebrovasodilation after brain injury.
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Editorial Comment Review
Cerebrovascular monitoring during carotid endarterectomy.
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Comparative Study
Serial MRI after transient focal cerebral ischemia in rats: dynamics of tissue injury, blood-brain barrier damage, and edema formation.
With the advent of thrombolytic therapy for acute stroke, reperfusion-associated mechanisms of tissue injury have assumed greater importance. In this experimental study, we used several MRI techniques to monitor the dynamics of secondary ischemic damage, blood-brain barrier (BBB) disturbances, and the development of vasogenic edema during the reperfusion phase after focal cerebral ischemia in rats. ⋯ Reperfusion after short periods of ischemia (30 to 60 minutes) appears to be mainly complicated by secondary ischemic damage as shown by the delayed recurrence of the DWI lesions, whereas BBB damage associated with vasogenic edema becomes a dominant factor with longer occlusion times (2.5 hours).
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Comparative Study
Effects of delayed intraischemic and postischemic hypothermia on a focal model of transient cerebral ischemia in rats.
Intraischemic mild hypothermia has been shown to be neuroprotective in reducing cerebral infarction in transient focal ischemia. As a more clinical relevant issue, we investigated the effect of delayed intraischemic and postischemic hypothermia on cerebral infarction in a rat model of reversible focal ischemia. We also examined the effect of hypothermia on the inflammatory response after ischemia-reperfusion to assess the neuroprotective mechanism of brain hypothermia. ⋯ Ischemic brain damage can be reduced with delayed intraischemic and prolonged postischemic hypothermia in a focal model of transient cerebral ischemia in rats. The neuroprotective mechanism of hypothermia may be mediated by suppression of PMNL-mediated inflammatory response after ischemia-reperfusion in this model.
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Multicenter Study Comparative Study
Association of intraoperative transcranial doppler monitoring variables with stroke from carotid endarterectomy.
The outcomes of carotid endarterectomy (CEA) are, in addition to patient baseline characteristics, highly dependent on the safety of the surgical procedure. During the successive stages of the operation, transcranial Doppler (TCD) monitoring of the middle cerebral artery (MCA) was used to assess the association of cerebral microembolism and hemodynamic changes with stroke and stroke-related death. ⋯ In CEA, TCD-detected microemboli during dissection and wound closure, > or =90% MCA velocity decrease at cross-clamping, and > or =100% pulsatility index increase at clamp release are associated with operative stroke. In combination with the presence of preoperative cerebral symptoms and > or =70% ipsilateral internal carotid artery stenosis, these 4 TCD monitoring variables reasonably discriminate between patients with and without operative stroke. This supports the use of TCD as a potential intraoperative monitoring modality to alter the surgical technique by enhancing a decrease of the risk of stroke during or immediately after the operation.