Acta neurochirurgica. Supplement
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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
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
Cerebral Arterial Time Constant Recorded from the MCA and PICA in Normal Subjects.
Cerebral arterial time constant (τ) estimates how quickly the cerebral arterial bed distal to the point of insonation is filled with arterial blood following a cardiac contraction. It is not known how τ behaves in different vascular territories in the brain. We therefore investigated the differences in τ of two cerebral arteries: the posterior inferior cerebellar artery (PICA) and the middle cerebral artery (MCA). ⋯ The MCA-supplied vascular bed has a longer distal average length, measured from the place of insonation up to the small arterioles, than the PICA-supplied vascular bed. Therefore, a longer time is needed to fill it with arterial blood volume. This study thus confirms the physiological validity of the τ concept.
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We studied possible correlations between cerebral hemodynamic indices based on critical closing pressure (CrCP) and cerebrospinal fluid (CSF) compensatory dynamics, as assessed during lumbar infusion tests. Our data consisted of 34 patients with normal-pressure hydrocephalus who undertook an infusion test, in conjunction with simultaneous transcranial Doppler ultrasonography (TCD) monitoring of blood flow velocity (FV). CrCP was calculated from the monitored signals of ICP, arterial blood pressure (ABP), and FV, whereas vascular wall tension (WT) was estimated as CrCP - ICP. ⋯ CM at baseline correlated inversely with brain elasticity (R = -0.358; p = 0.038). Neither CrCP nor WT correlated with CSF compensatory parameters. Overall, CrCP increases and WT decreases during infusion tests, whereas CM at baseline pressure may act as a characterizing indicator of the cerebrospinal compensatory reserve.
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Acta Neurochir. Suppl. · Jan 2016
Cannabinoid Receptor Type 2 Agonist Attenuates Acute Neurogenic Pulmonary Edema by Preventing Neutrophil Migration after Subarachnoid Hemorrhage in Rats.
We evaluated whether JWH133, a selective cannabinoid type 2 receptor (CB2R) agonist, prevented neurogenic pulmonary edema (NPE) after subarachnoid hemorrhage (SAH) by attenuating inflammation. Adult male rats were assigned to six groups: sham-operated, SAH with vehicle, SAH with JWH133 (0.3, 1.0, or 3.0 mg/kg) treatment 1 h after surgery, and SAH with JWH133 (1.0 mg/kg) at 1 h with a selective CB2R antagonist, SR144528 (3.0 mg/kg). The perforation model of SAH was performed and pulmonary wet-to-dry weight ratio was evaluated 24 and 72 h after surgery. ⋯ SAH-induced increasing levels of myeloperoxidase (MPO) and decreasing levels of a tight junction (TJ) protein, junctional adhesion molecule (JAM)-A, were ameliorated by JWH133 (1.0 mg/kg) administration 24 h after SAH. Immunohistochemical assessment also confirmed substantial leukocyte infiltration in the outside of vessels in SAH, which were attenuated by JWH133 (1.0 mg/kg) injection. CB2R agonist ameliorated lung permeability by inhibiting leukocyte trafficking and protecting tight junction proteins in the lung of NPE after SAH.