Under global cerebral ischemia, the effect of different brain temperature on cerebral ischemic injury was studied. Male Sprague-Dawley rats were divided into normothermic (37-38°C) ischemia, mild hypothermic (31-32°C) ischemia, hyperthermic (41-42°C) ischemia and sham-operated groups. Global cerebral ischemia was established using the Pulsinelli four-vessel occlusion model and brain temperature was maintained at defined level for 60 min after 20-min ischemia. The expression of c-fos protein and the levels of malondialdehyde (MDA) and lactate in brain regions were detected by immunochemistry and spectrophotometrical methods, respectively. C-fos positive neurons were found in the hippocampus and cerebral cortex after cerebral ischemia reperfusion. Mild hypothermia increased the expression of c-fos protein in both areas, whereas hyperthermia decreased the expression of c-fos protein in the hippocampus at 24 h reperfusion, and the cerebral cortex at 48 h reperfusion when compared to normothermic conditions. In normothermic, mild hypothermic and hyperthermic ischemia groups, the levels of MDA and lactate in brain tissue were increased at 24, 48 and 72 h reperfusion following 20-min ischemia as compared with the sham-operated group (P<0.01). The levels of MDA and lactate in mild hypothermic group were significantly lower than those in normothermic group (P<0.01). It is suggested that brain temperature influences the translation of the immunoreactive protein product of c-fos after global cerebral ischemia, and MDA and lactate are also affected by hypothermia and hyperthermia.
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http://dx.doi.org/10.1007/s11596-014-1282-4 | DOI Listing |
BMC Neurol
January 2025
Department of Neurosurgery, Gifu University Graduate School of Medicine, 1-1, Yanagido, Gifu, 501-1194, Japan.
Background: Tyrosine kinase inhibitors (TKIs) improve prognosis in chronic myeloid leukemia (CML). Nilotinib and ponatinib, second- and third-generation TKIs, respectively, have been reported to cause adverse vascular occlusive events such as myocardial infarction and peripheral arterial disease. However, little is known about the risk of cerebral infarction associated with severe cerebrovascular stenosis, which is a late complication of TKIs.
View Article and Find Full Text PDFNeurosurg Rev
January 2025
Dow Medical College, Dow University of Health Sciences, Karachi, Pakistan.
Aneurysmal Subarachnoid Hemorrhage (aSAH), resulting from ruptured aneurysms, is a major contributor to stroke-related mortality and morbidity. Despite advances in healthcare, aSAH remains severe and often leads to complications such as cerebral vasospasm (CV), cerebral infarction, and delayed ischemic neurological deficits (DIND). Clazosentan, an endothelin receptor antagonist, has demonstrated potential in alleviating vasospasm and its associated outcomes, although evidence of its efficacy remains unclear.
View Article and Find Full Text PDFJ Neurointerv Surg
January 2025
Intervention Neuroradiology, CHU Limoges, Limoges, Aquitaine-Limousin-Poitou-Charentes, France
Background: Hemorrhage is a major complication of brain arteriovenous malformations (AVMs) embolization, which can be related to persistent arteriovenous shunts that were not completely occluded during the embolization. In transvenous embolization (TVE) this risk is deemed higher for AVMs larger than 3 cm featuring multiple veins of drainage. Herein, we will discuss a few selected cases where brain AVMs with more than one draining vein were deemed safe for curative embolization with advanced endovascular techniques after a careful anatomical study through the four dimensional-digital subtraction angiography (4D-DSA) imaging.
View Article and Find Full Text PDFClinics (Sao Paulo)
January 2025
Department of Pediatrics, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, South Korea. Electronic address:
Introduction: This study aimed to investigate the associations among seizures, clinical characteristics, and brain injury on Magnetic Resonance Imaging (MRI) in infants with Hypoxic Ischemic Encephalopathy (HIE), and to determine whether these findings can predict unfavorable neurodevelopmental outcomes.
Method: Clinical and electrographic seizures were assessed by amplitude-integrated electroencephalogram, and the extent of brain injury was evaluated by using MRI. At 12‒24 months of age, developmental impairment or death was assessed.
J Stroke Cerebrovasc Dis
January 2025
Department of Gerontology, The Affiliated Traditional Chinese Medicine Hospital of Southwest Medical University, Luzhou, 646000, China. Electronic address:
Objective: Hirudin has shown potential in promoting angiogenesis and providing neuroprotection in ischemic stroke; however, its therapeutic role in promoting cerebrovascular angiogenesis remains unclear. In this study, we aimed to investigate whether hirudin exerts neuroprotective effects by promoting angiogenesis through the regulation of the Wnt/β-catenin signaling pathway.
Methods: An in vitro model of glucose and oxygen deprivation/reperfusion (OGD/R) was established using rat brain microvascular endothelial cells (BMECs).
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