Acta neurochirurgica. Supplement
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Acta Neurochir. Suppl. · Jan 2016
Sevoflurane Preconditioning Confers Neuroprotection via Anti-apoptosis Effects.
Neuroprotection against cerebral ischemia afforded by volatile anesthetic preconditioning (APC) has been demonstrated both in vivo and in vitro, yet the underlying mechanism is poorly understood. We previously reported that repeated sevoflurane APC reduced infarct size in rats after focal ischemia. In this study, we investigated whether inhibition of apoptotic signaling cascades contributes to sevoflurane APC-induced neuroprotection. ⋯ APC with sevoflurane markedly decreased apoptotic cell death in rat brains, which was accompanied by decreased caspase-3 cleavage and cytochrome c release. The apoptotic suppression was associated with increased ratios of anti-apoptotic Bcl-2 family proteins over pro-apoptotic proteins and with decreased activation of JNK and p53 pathways. Thus, our data suggest that suppression of apoptotic cell death contributes to the neuroprotection against ischemic brain injury conferred by sevoflurane preconditioning.
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Acta Neurochir. Suppl. · Jan 2016
Intraventricular Injection of Noncellular Cerebrospinal Fluid from Subarachnoid Hemorrhage Patient into Rat Ventricles Leads to Ventricular Enlargement and Periventricular Injury.
Early brain injury and hydrocephalus (HCP) are important mediators of poor outcome in subarachnoid hemorrhage (SAH) patients. We aim to understand the development of HCP and subependymal cellular injury after intraventricular injection of noncellular human SAH cerebrospinal fluid (CSF) into rat ventricles. Two-hundred microliters of noncellular CSF from SAH patients or normal controls were injected into the right lateral ventricle of seven adult male Sprague-Dawley rats. ⋯ We found that the ventricular area at the bregma level in the CSF injection group was significantly larger than that in the control group (p < 0.05). The periventricular tissue in the CSF injection group had significantly more necrotic cell death as well as HO-1 expression as compared with the control group (p < 0.05). In conclusion, injection of SAH patients' CSF into the rat ventricle leads to HCP as well as subependymal injury compared with injection of control CSF.
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Acta Neurochir. Suppl. · Jan 2016
Retrograde Suction Decompression Through Direct Puncture of the Common Carotid Artery for Paraclinoid Aneurysm.
Surgical clipping of paraclinoid aneurysm can be very difficult because strong adhesions may hinder the dissection of the perforators and surrounding anatomical structures from the aneurysm dome. We describe our experience with using retrograde suction decompression during the clipping of paraclinoid aneurysms and discuss the relative advantages and pitfalls. ⋯ Retrograde suction decompression through direct puncture of the common carotid artery is a useful adjunct technique for the clipping of paraclinoid ICA aneurysms.
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Research suggests that early brain injury following subarachnoid hemorrhage (SAH) is a primary therapeutic target, and early SAH-induced basal ganglia injury is not well studied. The present study examined basal ganglia injury in a rat model of SAH. Adult male Sprague-Dawley rats (n = 78) weighing 275-300 g underwent endovascular perforation to mimic aneurysmal SAH. ⋯ Basal ganglia neuronal injury was also determined by examining the levels of dopamine- and cAMP-regulated phosphoprotein, Mr 32 kDa (DARPP-32). We found that rats with hydrocephalus had more severe basal ganglia injury with greater DARPP-32 depletion (DARPP-32/beta-actin: 0.38 ± 0.32 vs. 0.86 ± 0.45 in rats without hydrocephalus and 1.10 ± 0.28 in sham, p < 0.05). In conclusion, SAH resulted in severe basal ganglia damage, which is associated with hydrocephalus development.
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Acta Neurochir. Suppl. · Jan 2015
ReviewNeurovascular events after subarachnoid hemorrhage: focusing on subcellular organelles.
Subarachnoid hemorrhage (SAH) is a devastating condition with high morbidity and mortality rates due to the lack of effective therapy. Early brain injury (EBI) and cerebral vasospasm (CVS) are the two most important pathophysiological mechanisms for brain injury and poor outcomes for patients with SAH. CVS has traditionally been considered the sole cause of delayed ischemic neurological deficits after SAH. ⋯ The dysfunction of subcellular organelles, such as endoplasmic reticulum stress, mitochondrial failure, and autophagy-lysosomal system activation, has developed during EBI and delayed brain injury after SAH. To our knowledge, there is a lack of review articles addressing the direction of organelle dysfunction after SAH. In this review, we discuss the roles of organelle dysfunction in the pathogenesis of SAH and present the opportunity to develop novel therapeutic strategies of SAH via modulating the functions of organelles.