Stroke; a journal of cerebral circulation
-
Intraventricular extension of hemorrhage is a predictor of poor outcome in intracerebral hemorrhage, and iron overload contributes to brain injury after intracerebral hemorrhage. The current study investigated the role of iron in ventricular dilatation and neuronal death in a rat model of intraventricular hemorrhage (IVH). ⋯ Iron has a role in brain injury after IVH. Deferoxamine may be a therapy for patients with IVH or intraventricular extension after intracerebral hemorrhage.
-
Comparative Study
Pharmacologically augmented S-nitrosylated hemoglobin improves recovery from murine subarachnoid hemorrhage.
S-nitrosylated hemoglobin (S-nitrosohemoglobin) has been implicated in the delivery of O(2) to tissues through the regulation of microvascular blood flow. This study tested the hypothesis that enhancement of S-nitrosylated hemoglobin by ethyl nitrite inhalation improves outcome after experimental subarachnoid hemorrhage (SAH). ⋯ Targeted S-nitrosylation of hemoglobin improved outcome parameters, including vessel diameter, tissue blood flow, cortical tissue Po(2), and neurologic function in a murine SAH model. Augmenting endogenous Po(2)-dependent delivery of NO bioactivity to selectively dilate the compromised cerebral vasculature has significant clinical potential in the treatment of SAH.
-
Comparative Study
Cyclooxygenase-2 mediates hyperbaric oxygen preconditioning in the rat model of transient global cerebral ischemia.
Hyperbaric oxygen (HBO) preconditioning (PC) allows brain protection against transient global ischemia. In the present study, we hypothesize that the mechanism of HBO-PC involves the induction of cyclooxygenase-2 (COX-2) in cerebral tissues before ischemia, which leads to a suppression of COX-2 and its downstream targets after global ischemic insult. ⋯ HBO-PC reduced COX-2 expression and provided brain protection after global ischemia. Administration of COX-2 inhibitor with HBO before ischemia abolished preconditioning effect, thereby implicating COX-2 as a mediator of HBO-PC in the ischemic brain.
-
Comparative Study
Preservation of tropomyosin-related kinase B (TrkB) signaling by sodium orthovanadate attenuates early brain injury after subarachnoid hemorrhage in rats.
Recent studies reported that apoptosis was involved in the pathogenesis of early brain injury after subarachnoid hemorrhage (SAH). The aim of this study was to examine whether sodium orthovanadate (SOV) prevents post-SAH apoptosis by modulating growth factors and its downstream receptor tyrosine kinases. Method- Rats were operated on with the endovascular perforation model. SAH animals were treated with vehicle, 3 mg/kg and 10 mg/kg SOV, and evaluated regarding neurofunction and brain edema. The expression of growth factors such as mature brain-derived neurotrophic factor, insulin-like growth factor-1, and vascular endothelial growth factor and phosphorylation of tropomyosin-related kinase B, which is a receptor tyrosine kinase for brain-derived neurotrophic factor and the downstream pathway in antiapoptosis, was examined by Western blot analysis. Neuronal cell death was measured with terminal deoxynucleotidyl transferase-mediated uridine 5'-triphosphate-biotin nick end-labeling staining. We also administered K252a, a tropomyosin-related kinase B antagonist, to examine the mechanisms for neuroprotective effects by SOV. ⋯ The current study showed that brain-derived neurotrophic factor-induced tropomyosin-related kinase B activation by SOV was necessary for protection against early brain injury after SAH.