Double Injection Model Research Articles

High responsive Pd decorated low temperature α-MoO3 hydrogen gas sensor

The H2 gas adsorption properties, which are the most crucial concept for a gas sensor, of the 2-dimensional (2D) MoS2 are limited compared to its oxide form of 2D α-MoO3. On the other hand, it is straightforward to form high surface-to-volume ratio nanostructures with MoS2. In order to get the benefits of the large surface and better H2 adsorption properties for the H2 gas sensor, MoS2 film grown by the chemical vapor deposition (CVD) method was converted into MoO3 with a thermal oxidation process at 380 °C under oxygen-ambient conditions. The grown MoS2 film has indicated that it is formed from the coalesced MoS2 flakes. An ultra-high response of 3 × 106 at a relatively low temperature of 100 °C was achieved for as low as 800 ppm hydrogen concentration. The hydrogen gas sensing mechanism has been discussed in depth using the double injection model, similar to the electrochromic mechanism.

Effect of Vasa Vasorum on Basilar Artery Vasospasm Following Subarachnoid Hemorrhage

A well-documented association exists between the vasa vasorum and vasopathologies, including atherosclerosis. However, information on the role of the vasa vasorum during vascular degenerative changes of vasospasm after subarachnoid hemorrhage (SAH) is insufficient. In this study, 34 rabbits were divided into 3 groups: basal group (N= 8), sham group (N= 8), and SAH group (N= 18). Experimental SAH was formed using a double-injection model. During follow-up, the neurologic status of the rabbits was observed. All rabbits were euthanized after 2 weeks, and the vasopathologic degeneration was categorized as normal, mild, moderate, and severe according to the changes in the basilar arteries. The numbers, locations, and spasms of the vasa vasorum and their relation to the vasodegenerative changes of the basilar artery were investigated. The basilar arteries were graded as normal in the basal and sham groups. In the SAH group, 6 rabbits had mild, 7 had moderate, and 5 had severe degeneration. Neurologic deficits were prominent in the SAH group, and deficit grades correlated with vascular degeneration. The number of the vasa vasorum were significantly higher in the SAH group, and an enhanced formation of the vasa vasorum was noted in which severe degenerative changes were present. Moreover, the vasospasm index of the vasa vasorum, which increased with the aggravation of vascular degenerative changes, was significantly higher in the SAH group. The vasa vasorum and their vasospasm play a crucial role in the pathogenesis of basilar artery degeneration in the vasospasm following SAH.

AC Electroluminescent Processes in Pr3+-Activated (Ba0.4Ca0.6)TiO₃ Diphase Polycrystals.

We investigated the properties of alternating current (AC)-driven electroluminescence from (Ba0.4Ca0.6)TiO3:Pr3+ diphase polycrystal-based device. The results of crystal phases and micrographs, and the symmetrical dual emissions in one AC cycle, indicate the spontaneous formation of a dielectric/phosphor/dielectric sandwich microstructure in (Ba0.4Ca0.6)TiO3:Pr3+. The electroluminescent device emits a red light of 617 nm, which is attributed to the 1D2-3H4 transition of Pr3+ in the phosphor phase. At a fixed AC frequency, the intensity of electroluminescence exhibits a steep enhancement when applying an increased driving electric field that is beyond a threshold. In a fixed driving electric field, the intensity of electroluminescence shows a rapid rise at low frequencies, but reaches saturation at high frequencies. Based on a double-injection model, we discussed systematically the electroluminescent processes in a whole cycle of AC electric field, which matched well with the experimental data. Our investigation is expected to expand our understanding of such a diphase electroluminescent device, thereby promoting their applications in lighting and displays.

Long-Lasting Cerebral Vasospasm, Microthrombosis, Apoptosis and Paravascular Alterations Associated with Neurological Deficits in a Mouse Model of Subarachnoid Hemorrhage.

Subarachnoid hemorrhage (SAH) is a devastating disease with high mortality and morbidity. Long-term cognitive and sensorimotor deficits are serious complications following SAH but still not well explained and described in mouse preclinical models. The aim of our study is to characterize a well-mastered SAH murine model and to establish developing pathological mechanisms leading to cognitive and motor deficits, allowing identification of specific targets involved in these long-term troubles. We hereby demonstrate that the double blood injection model of SAH induced long-lasting large cerebral artery vasospasm (CVS), microthrombosis formation and cerebral brain damage including defect in potential paravascular diffusion. These neurobiological alterations appear to be associated with sensorimotor and cognitive dysfunctions mainly detected 10days after the bleeding episode. In conclusion, this characterized model of SAH in mice, stressing prolonged neurobiological pathological mechanisms and associated sensitivomotor deficits, will constitute a validated preclinical model to better decipher the link between CVS, long-term cerebral apoptosis and cognitive disorders occurring during SAH and to allow investigating novel therapeutic approaches in transgenic mice.

Recombinant osteopontin attenuates experimental cerebral vasospasm following subarachnoid hemorrhage in rats through an anti-apoptotic mechanism

Cerebral vasospasm (CVS) is an important pathological process following subarachnoid hemorrhage (SAH). Osteopontin (OPN), a pleiotropic extracellular glycoprotein, has been reported to be able to induce MKP-1 in the spastic cerebral arteries and prevent vasospasm after SAH. The purpose of this study was to investigate the protective effects of recombinant OPN (r-OPN) on CVS following SAH and the underlying mechanisms associated with its anti-apoptotic effect. Eighty male Sprague Dawley rats (weighing 300–375g) were randomly assigned to four groups: (1) sham+vehicle (n=20), (2) SAH+vehicle (n=20), (3) SAH+OPN0.03 (0.03μg) (n=20), (4) SAH+OPN0.1 (0.1μg) (n=20). The double injection model of cisterna magna was performed on day 0 and 48h after the first induction. r-OPN was administered intraventricularly nearly 30min after the first SAH. After neurological score assessment, rats were sacrificed 72h after the first SAH. The cross-sectional area and thickness of basilar arteries (BA) were measured under Hematoxylin–eosin (H&E) staining. Endothelial cell apoptosis was identified by terminal deoxynucleotidyl transferase mediated nick end labeling (TUNEL) staining. Immunohistochemistry was used to assess the expression of p-Akt and cleaved caspase-3 in BA. Western blot analysis was applied to evaluate the expression of p-Akt, cleaved caspase-3, Bax and Bcl-2 in BA. r-OPN improved neurological scores and attenuated vasospasm. r-OPN significantly reduced expression of cleaved caspase-3 and Bax in BA following SAH, and increased the level of p-Akt and Bcl-2, coupled with reduced apoptosis of endothelial cell in BA. These results demonstrate that r-OPN can attenuate vasospasm after SAH through a suppressed apoptotic response, which may provide a novel therapeutic target for cerebral vasospasm.

Research Progress in Gasochromics Mechanism of Tungsten Oxide Thin Films

The gasochromic effect and its potential applications of tungsten oxide (WO3) thin films are introduced. The research progress in gasochromics mechanism of WO3films is reviewed and various mechanism models are summarized and discussed. The double injection model, oxygen vacancy diffusion model and localized water molecules model are extensively used to explain the gasochromic coloration of WO3films. A perspective on the gasochromics mechanism development of WO3films is tended to fabricate WO3film with single crystal and regular structure, which may simply the quantitative characterizations induced by the complicated structure. Elucidating gasochromics mechanism of WO3films not only helps to understand gasochromic coloration phenomenon well but also improves the performance of gasochromic coloration devices. It also accelerates the development of the relative science, such as gas detector, atom/ion transport material, surface catalysis of semiconductor, and so on.

Possible Role of Raf-1 Kinase in the Development of Cerebral Vasospasm and Early Brain Injury After Experimental Subarachnoid Hemorrhage in Rats.

This study aims to clarify the potential role of Raf-1 kinase in cerebral vasospasm (CVS) and early brain injury (EBI) after subarachnoid hemorrhage (SAH). Two experimental SAH models in rats, including cisterna magna double injection model for CVS study and prechiasmatic cistern single injection model for EBI study, were performed in this research. As a specific inhibitor of Raf-1, BAY 43-9006 was used in this study. In CVS study, time course study showed that the basilar artery exhibited vasospasm after SAH and became most severe at day 5, and the phosphorylation of Raf-1 had the same trends, while both vasospasm and the phosphorylation of Raf-1 induced by SAH were inhibited by BAY 43-9006 treatment. In addition, BAY 43-9006 treatment significantly reversed the phosphorylation of ERK1/2 and the activation of NF-κB induced by SAH and decreased the messenger RNA (mRNA) levels of IL-6 and IL-1β. In EBI study, BAY 43-9006 treatment significantly suppressed the brain injury induced by SAH. Besides, BAY 43-9006 inhibited the phosphorylation of Raf-1 and ERK1/2; decreased the protein levels of COX-2, VEGF, and MMP-9; and reversed the activation of NF-κB induced by SAH. These results demonstrate that Raf-1 kinase contributes to CVS and EBI after SAH by enhancing the activation of the Raf-1/ERK1/2 and Raf-1/NF-κB signaling pathways, and that the inhibition of these pathways might offer new treatment strategies for CVS and EBI.

Rat cisterna magna double-injection model of subarachnoid hemorrhage - background, advantages/limitations, technical considerations, modifications, and outcome measures.

The pathophysiological changes following aneurysmal subarachnoid hemorrhage (SAH) are commonly divided into early consequences (developing shortly after the bleeding) and delayed consequences of the bleeding. The development of delayed injury mechanisms, e.g., reduced cerebral blood flow (CBF) caused by cerebral vasospasm (CVS) or development of delayed ischemic neurological deficits (DIND), seem mainly to depend on the amount and duration of the subarachnoid blood clot. CVS may progress to cerebral ischemia and infarction, and therefore lead to delayed neurological deterioration. The rat double-hemorrhage model reproduces the time course of the delayed pathophysiological consequences of CVS, which imitates the clinical setting more precisely than other rodent models. Furthermore, this model is adjustable via various technical considerations or modifications. Therefore, the double-hemorrhage model is predisposed to be used to mimic the delayed effects of SAH and to investigate the use of drugs on morphological ischemic, functional, and vasospastic effects.

Common carotid artery occlusion combined with double subarachnoid hemorrhage for modifying cerebral vasospasm model

Objective To establish an animal model with more serious ischemic brain damage by combining unilateral carotid artery ligation with double injection model of cisterna magna.Methods Thirty New Zealand rabbits were evenly randomized into sham group,subarachnoid hemarrhage(SAH)group,and SAH + carotid artery occlusion(CAO)group.Double blood injection was performed in SAH group and SAH+CAO group;right carotid artery ligation was also performed in the SAH+CAO group.All the animals were sacrificed at day 5after the first blood injection,and then H-E and TUNEL staining were performed for the brain tissue sections.The diameter of the basilar artery was measured and the neuronal apoptosis was counted at the hippocampus region.Results The survival rate for the sham group,SAH group,and SAH+CAO group were 100%,90%,and 70%,respectively.Compared with the sham group,SAH group and SAH+CAO group had significant basilar artery vasospasm and neural apoptosis(P0.001).The diameters of basilar artery were not significantly different between SAH group and SAH+CAO group(P=0.342);however,the neuronal apoptosis count in hippocampal region was significantly higher in SAH+CAO group than in SAH group(P=0.005).Conclusion Unilateral carotid artery ligation combined with double injection model of cisterna magna can be used to establish a more serious cerebral vasospasm model.

Nuclear factor‐κB/Bcl‐XL pathway is involved in the protective effect of hydrogen‐rich saline on the brain following experimental subarachnoid hemorrhage in rabbits

Early brain injury (EBI), a significant contributor to poor outcome after subarachnoid hemorrhage (SAH), is intimately associated with neuronal apoptosis. Recently, the protective role of hydrogen (H2 ) in the brain has been widely studied, but the underlying mechanism remains elusive. Numerous studies have shown nuclear factor-κB (NF-κB) as a crucial survival pathway in neurons. Here we investigated the role of H2 in EBI following SAH, focusing on the NF-κB pathway. A double blood injection model was used to produce experimental SAH, and H2 -rich saline was injected intraperitoneally. NF-κB activity within the occipital cortex was measured. Immunofluorescence was performed to demonstrate the activation of NF-κB; Bcl-xL and cleaved caspase-3 were determined via Western blot. Gene expression of Bcl-xL was detected by real-time PCR, and TUNEL and Nissl staining were performed to illustrate brain injury in the occipital cortex. SAH induced a significant increase of cleaved caspase-3. Correspondingly, TUNEL staining demonstrated obvious neuronal apoptosis following SAH. In contrast, H2 treatment markedly increased NF-κB activity and the expression of Bcl-xL and decreased the level of cleaved caspase-3. Additionally, H2 treatment significantly reduced post-SAH neuronal apoptosis. The current study shows that H2 treatment alleviates EBI in the rabbits following SAH and that NF-κB/Bcl-xL pathway is involved in the protective role of H2 .

Experimental high-altitude intracerebral hemorrhage in minipigs: histology, behavior, and intracranial pressure in a double-injection model

Specific pathophysiological mechanism in intracerebral hemorrhage (ICH) at high altitude is unclear, and at present, there is no relevant and suitable animal model. A hypobaric chamber was used to simulate an altitude of 4,000 m. Autologous arterial blood (3 ml) was slowly infused into the right basal ganglia of minipigs by a double-injection method for producing ICH. The intracranial pressure and neurological score of the high-altitude group were significantly higher than those of the low-altitude (plain) group. The brain water contents and pathological lesions of perihematoma tissue were more severe in the high-altitude group. The injury resulting from ICH at high altitude was more severe than that in the plain group. This model was able to produce controllable and reproducible hematomas and visible neurological deficits, which may be useful for future studies of the pathophysiology and functional rehabilitation of high-altitude ICH disease.

A modified double injection model of cisterna magna for the study of delayed cerebral vasospasm following subarachnoid hemorrhage in rats

Delayed cerebral vasospasm following subarachnoid hemorrhage (SAH) is a serious medical complication, characterized by constriction of cerebral arteries leading to varying degrees of cerebral ischemia. Numerous clinical and experimental studies have been performed in the last decades; however, the pathophysiologic mechanism of cerebral vasospasm after SAH still remains unclear. Among a variety of experimental SAH models, the double hemorrhage rat model involving direct injection of autologous arterial blood into the cisterna magna has been used most frequently for the study of delayed cerebral vasospasm following SAH in last years. Despite the simplicity of the technique, the second blood injection into the cisterna magna may result in brainstem injury leading to high mortality. Therefore, a modified double hemorrhage model of cisterna magna has been developed in rat recently. We describe here step by step the surgical technique to induce double SAH and compare the degree of vasospasm with other cisterna magna rat models using histological assessment of the diameter and cross-sectional area of the basilar artery.

The neuro-behavioral profile in rats after subarachnoid hemorrhage

Despite significant advancements in the understanding of the pathophysiological mechanisms of subarachnoid hemorrhage (SAH), little is known about the emotional consequences. The primary goal of this study was to describe the locomotor and behavioral patterns in rats following both a single-injection and double-injection model of SAH. In 48 rats, SAH was induced by injecting 0.3ml of autologous arterial blood into the cisterna magnum (single-hemorrhagic model). In 24 of these rats, post-SAH vasospasm was induced by a repeated injection of blood into the cisterna magnum 24h later (double-hemorrhagic model). In 24 additional rats, 0.3ml of saline was injected into the cisterna magnum (sham group). Neurological performance was assessed at 24, 48h, 1, 2 and 3 weeks after SAH. Four behavioral tests were performed for 3 weeks after SAH for the duration of 6 consequent days, in the following order: open field test, sucrose preference test, elevated plus maze test and forced swimming test. Following both, a single and double-hemorrhagic models of SAH, rats were found to have significant behavioral abnormalities on the open field test, sucrose preference test, elevated plus maze test, and forced swimming test. A more prominent disability was found in rats that underwent the double-hemorrhagic model of SAH than rats that underwent the single-hemorrhagic model. Both a single and double injection model of rats SAH are associated with significant behavioral disturbances including locomotor abnormalities, depressive behavior and increased anxiety, even as early as 3 weeks after SAH.

Modeling Intracerebral Hemorrhage in Mice: Injection of Autologous Blood or Bacterial Collagenase

Spontaneous intracerebral hemorrhage (ICH) defines a potentially life-threatening neurological malady that accounts for 10-15% of all stroke-related hospitalizations and for which no effective treatments are available to date(1,2). Because of the heterogeneity of ICH in humans, various preclinical models are needed to thoroughly explore prospective therapeutic strategies(3). Experimental ICH is commonly induced in rodents by intraparenchymal injection of either autologous blood or bacterial collagenase(4). The appropriate model is selected based on the pathophysiology of hemorrhage induction and injury progression. The blood injection model mimics a rapidly progressing hemorrhage. Alternatively, bacterial collagenase enzymatically disrupts the basal lamina of brain capillaries, causing an active bleed that generally evolves over several hours(5). Resultant perihematomal edema and neurofunctional deficits can be quantified from both models. In this study, we described and evaluated a modified double injection model of autologous whole blood(6) as well as an ICH injection model of bacterial collagenase(7), both of which target the basal ganglia (corpus striatum) of male CD-1 mice. We assessed neurofunctional deficits and brain edema at 24 and 72 hr after ICH induction. Intrastriatal injection of autologous blood (30 μl) or bacterial collagenase (0.075U) caused reproducible neurofunctional deficits in mice and significantly increased brain edema at 24 and 72 hr after surgery (p<0.05). In conclusion, both models yield consistent hemorrhagic infarcts and represent basic methods for preclinical ICH research.

Growth of Ge1 − x Sn x solid solution films and study of their structural properties and some of their photoelectric properties

From the charge state and closeness of the covalent radii of molecules of the solution-forming components, the possibility of the formation of the solutions Si1 − xGex, Si1 − xSnx, (Si2)1 − x(SnC)x, Ge1 − xSnx, (Ge2)1 − x(SiSn)x, (SiC)1 − x(GeC)x, (GeC)1 − x(SnC)x, and (SiGe)1 − x(SnC)x based on chemical elements of Group IV has been predicted. Single-crystal films of the substitutional solid solution Ge1 − xSnx (0 ≤ x ≤ 0.03) have been grown on Ge substrates by liquid-phase epitaxy. X-ray diffraction patterns, spectral photosensitivity, and the I–V characteristics of the obtained n-Ge-p-Ge1 − xSnx heterostructures have been investigated. The lattice parameters of the epitaxial film and the substrate af = 5.6812 A and as = 5.6561 A have been determined. The spectral photosensitivity of the n-Ge-p-Ge1 − xSnx heterostructures encompasses the photon energy range from 0.4 to 1.4 eV. It is shown that the forward portion of the I–V characteristics of the investigated structures at low voltages (up to 0.5 V) is described by the exponential dependence I = I0exp(qV/ckT) and at high voltages (V > 0.5 V), by the power dependence I ∝ Vα with the values α = 2 at V = (0.5–0.9) V, α = 1.3 at V = (0.9–1.4) V, and α = 2 at V > 1.4 V. The experimental data are explained within the double injection model for the n-p-p structure using the drift mechanism of current transport in the ohmic relaxation mode taking into account the inertia of the electron exchange inside a recombination complex.

Growth of (GaAs)1 − x (ZnSe) x solid solution films and investigation of their structural and some photoelectric properties

Single-crystal films of the substitutional solid solution (GaAs)1 − x(ZnSe)x (0 ≤ x ≤ 0.80) on GaAs substrates have been grown using liquid phase epitaxy. The X-ray diffraction patterns, photoluminescence spectra, and current-voltage characteristics of the n-(GaAs)-p-(GaAs)1 − x(ZnSe)x (0 ≤ x ≤ 0.80) heterostructures prepared have been investigated. The lattice parameters of the film af = 5.6544 A and the substrate as = 5.6465 A have been determined, and the profile of the molecular distribution of the solid solution components has been obtained. The photoluminescence spectrum of the (GaAs)1 − x(ZnSe)x (0 ≤ x ≤ 0.80) films exhibits a narrow peak (against the background of the broad luminescence band) with a maximum in the luminescence intensity at a photon energy of 2.67 eV due to the presence of Zn-Se bonds in the structure (ZnSe is covalently bonded to the tetrahedral lattice of the GaAs matrix). It has been shown that the direct branch of the current-voltage characteristics of the structures under investigation is described by an exponential dependence I = I0exp(qV/ckT) at low voltages (V > 0.3 V) and by a power-law dependence I ∼ Vα with exponents α = 4 at V = 0.4–0.8 V, α = 2 at V = 0.8–1.4 V, and α = 1.5 at V > 2 V. The experimental results have been explained in the framework of the double-injection model for the n-p-p+ structure under the condition that the concentration distribution of nonequilibrium charge carriers has a minimum.

Ferrous Chelator 2,2′-Dipyridyl Attenuates Cerebral Vasospasm after Experimental Subarachnoid Haemorrhage in Rabbits

The effect of 2,2'-dipyridyl (DP) on cerebral vasospasm was investigated in a double-injection rabbit model of subarachnoid haemorrhage (SAH). Thirty-six animals were divided between four groups: control (sham-operated), SAH (model alone), SAH + DP (the SAH model in which DP dissolved in dimethyl sulphoxide [DMSO] was injected once daily for 5 days into the cisterna magna), and SAH + DMSO (the SAH model in which DMSO [vehicle] was injected daily for 5 days). There were significant differences in the basilar artery luminal area, wall thickness, neurological deficit score and vasospasm index between the SAH + DP and SAH groups. There was a significant negative correlation between arterial luminal area and arterial wall thickness, and also between the neurological deficit score and vasospasm index. Cells that were positive for terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labelling (TUNEL) and p53 expression were significantly increased in the SAH + DMSO and SAH groups, but not in the SAH + DP group, versus controls. Thus, DP may attenuate cerebral vasospasm after SAH by suppressing p53-induced apoptosis in the cerebral vessels.

A double-injection model of intracerebral hemorrhage in rabbits

We aimed to develop a double-injection model of intracerebral hemorrhage (ICH) in rabbits and to evaluate it as a tool for investigating post-ICH brain injury. Rabbits were injected with 300 μL fresh autologous whole blood into the right basal ganglia. Behavioral changes were rated, brain water content (BWC) was measured and brain tissue morphology was also examined. ICH was established in 93.5% of the blood injection group. At 1, 3 and 7 days after ICH, there were significant differences in the total neurological scores ( p < 0.01) and BWC ( p < 0.01) between a sham-operated group and the ICH group. These findings suggest that the model produces a persistent neurological deficit, hematoma volume and perihematomal edema and closely mimics human hypertensive basal ganglia ICH; it is a controllable and reproducible hematoma that lends itself to quantitative investigation.

MRI of the Perihemorrhagic Zone in a Rat ICH Model: Effect of Hematoma Evacuation

Perihemorrhagic pathophysiology of spontaneous intracerebral hemorrhages (ICH) remains unclear. Recently, ischemic changes in the perihemorrhagic zone (PHZ) have been discussed as a potential source of secondary damage. In this study, we focussed on diffusion and perfusion characteristics of experimental ICH. Experimental ICH was induced with a double injection model in rats. In total, 49 animals were examined at three timepoints within 3.5 h after ICH with a 2.35T animal scanner. We investigated perihemorrhagic relative apparent diffusion coefficients (rADC) and relative mean transit time (rMTT). Animals were divided into 2 groups; controls (gr1, n = 27) and facilitated hematoma evacuation with recombinant tissue plasminogen activator (rt-PA) after the first of 3 imaging time points (gr2, n = 22). Diffusion (rADC) and perfusion (rMTT) characteristics were analyzed in 3 regions of interest surrounding the hematoma (ROI1-3). Overall rADC and rMTT values in ROI3 (normal tissue) did not show any changes. There was mild edema--not ischemia--in ROIs1 and 2 at TP1 with rADC of 1.05-1.18 in both groups indicating vasogenic edema (not ischemia). This did not change with hematoma evacuation. There was mild (non-critical) perfusion reduction in ROIs1 and 2 at TP1, which disappeared after clot evacuation in group 2 (P < 0.05 for TP3). Multifactorial ANOVA showed a solid trend (0.06 < P < 0.1) for clot evacuation associated normalization of perfusion in ROIs 1 and 2 within and in between groups 1 and 2. We demonstrated vasogenic edema and mild perfusion reduction in the PHZ above the ischemic threshold. The existence of a perihemorrhagic "penumbra" indicating critically ischemic tissue analogous to ischemic stroke is unlikely.

EFFECTS OF DEFEROXAMINE-ACTIVATED HYPOXIA-INDUCIBLE FACTOR-1 ON THE BRAINSTEM AFTER SUBARACHNOID HEMORRHAGE IN RATS

Hypoxia-inducible factor (HIF)-1 is a transcription factor that regulates the expression of various neuroprotective genes. The goal of this study was to clarify the relationship between HIF-1 expression and subarachnoid hemorrhage (SAH) and to characterize the effects of deferoxamine (DFO)-induced increases in HIF-1 protein levels on the brainstem and the basilar artery (BA) after experimental SAH. Rat single- and double-hemorrhage models (injected on Days 0 and 2) of SAH were used. We assessed the time courses for HIF-1 protein levels in the brainstems and the BA diameters within 10 minutes and 6 hours on Days 1 and 2 in the single-SAH model, and also on Day 7 in the double-SAH model. After induction of double hemorrhage in rats, DFO was injected intraperitoneally. We then evaluated HIF-1 protein expression and brainstem activity, BA diameter, and brainstem blood flow. After the rats experienced SAH, HIF-1 protein expression was significantly greater at 10 minutes in the single-injection model and at 7 days in the double-injection model than at similar time points in the control group, and these increases correlated with degrees of cerebral vasospasm. DFO injection resulted in significant increases in HIF-1 protein expression and activity in the brainstems of rats with SAH, compared with the rats with SAH that were given placebos, and the rats without SAH in the double-hemorrhage model. Cerebral vasospasm and reduction of brainstem blood flow were significantly attenuated in the rats that were administered DFO. These results show that a DFO-induced increase in HIF-1 protein level and activity exerts significant attenuation of BA vasospasm and reduction of brainstem blood flow in the rat model of SAH. DFO may be a promising agent for treating clinical SAH.