Vasospasm Model Research Articles

Comment on, “Gene expression in a canine basilar artery vasospasm model: a genome-wide network-based analysis”

Comment on, “Gene expression in a canine basilar artery vasospasm model: a genome-wide network-based analysis”

Vasodilatory effects of tadalafil in an animal model of cerebral vasospasm: Comparative analysis with oral nimodipine

ObjectivesCerebral vasospasm is one of the most fatal complications after spontaneous aneurysmal subarachnoid hemorrhage. Although various treatments have been tried for the treatment of cerebral vasospasm so far, the effect is insignificant or temporary except for oral nimodipine. Phosphodiesterase isozyme type 5 inhibitor, which is used to treat erection dysfunction, recently has been known to have a cerebrovascular vasodilation. It is thought that this will be effective in cerebral vasospasm, and the effect will be compared and analyzed with oral nimodipine through an animal model of cerebral vasospasm. Material and MethodsA total of 40 rabbits were used to make subarachnoid hemorrhage model and were divided into three groups - a control group, nimodipine group, and tadalafil group. The cerebral vessels were angiographically measured before and on the third day of subarachnoid hemorrhage. Then vertebrobasilar arteries were harvested and evaluated. Under the microscope, lumen area and media area were measured for each group and were compared. ResultsAngiographically, tadalafil group showed significant vasodilation compared with the control group (p < 0.01). Histologically, tadalafil showed a similar effect on lumen and on media area to that of nimodipine group compared with the control group. ConclusionsCerebral vasospasm could leave neurologic deficit or sequelae even after proper treatment. Therefore, prevention is important. Tadalafil showed preventive effect against cerebral vasospasm and vasodilative effect similar to that of nimodipine. Therefore, tadalafil could be considered an alternative preventive treatment of cerebral vasospasm.

Retracted: Predictive Model of Cerebral Vasospasm in Subarachnoid Hemorrhage Based on Regression Equation.

[This retracts the article DOI: 10.1155/2022/3397967.].

Effect of Cilostazol in Animal Models of Cerebral Ischemia and Subarachnoid Hemorrhage: A Systematic Review and Meta-Analysis.

Cilostazol, a phosphodiesterase III inhibitor, appears to be a promising agent for preventing cerebral ischemia in patients with aneurysmal subarachnoid hemorrhage. Here, the authors perform a systematic review and meta-analysis to quantitatively assess the effects of cilostazol on brain structural and functional outcomes in animal models of cerebral ischemia and subarachnoid hemorrhage-induced cerebral vasospasm. By using the PRISMA guidelines, a search of the PubMed, Scopus, and Web of Science was conducted to identify relevant studies. Study quality of each included study for both systematic reviews were scored by using an adapted 15-item checklist from the Collaborative Approach to Meta-Analysis of Animal Data from Experimental Studies. We calculated a standardized mean difference as effect size for each comparison. For each outcome, comparisons were combined by using random-effects modeling to account for heterogeneity, with a restricted maximum likelihood estimate of between-study variance. A total of 22 (median [Q1, Q3] quality score of 7 [5, 8]) and 6 (median [Q1, Q3] quality score of 6 [6, 6]) studies were identified for cerebral ischemia and subarachnoid hemorrhage-induced cerebral vasospasm, respectively. Cilostazol significantly reduced the infarct volume in cerebral ischemia models with a pooled standardized mean difference estimate of - 0.88 (95% confidence interval [CI] [- 1.07 to - 0.70], p < 0.0001). Cilostazol significantly reduced neurofunctional deficits in cerebral ischemia models with a pooled standardized mean difference estimate of - 0.66 (95% CI [- 1.06 to - 0.28], p < 0.0001). Cilostazol significantly improved the basilar artery diameter in subarachnoid hemorrhage-induced cerebral vasospasm with a pooled standardized mean difference estimate of 2.30 (95% CI [0.94 to 3.67], p = 0.001). Cilostazol also significantly improved the basilar artery cross-section area with a pooled standardized mean estimate of 1.88 (95% CI [0.33 to 3.43], p < 0.05). Overall, there was between-study heterogeneity and asymmetry in the funnel plot observed in all comparisons. Published animal data support the overall efficacy of cilostazol in reducing infarct volume and neurofunctional deficits in cerebral ischemia models and cerebral vasospasm in subarachnoid hemorrhage models.

Predictive Model of Cerebral Vasospasm in Subarachnoid Hemorrhage Based on Regression Equation.

In order to explore the regression equation for the prediction model of subarachnoid hemorrhage and cerebral vasospasm, the nomogram prediction model of SCVS occurrence was established. This study is a retrospective analysis of 125 cases of aSAH admitted to a hospital; the patients were divided into SCVS group and non-SCVS group. Select SIRI as a simple and reliable marker of inflammation, analyze its correlation with SCVS and its predictive value, and analyze the predictive value of SIRI to SCVS through ROC curve. Based on the SIRI inflammation level and other related risk factors, a nomogram prediction model for the occurrence of SCVS was built. The experimental results show that the SIRI level of patients in the SCVS group was significantly higher than that of the non-SCVS group, and logistic regression analysis found that SIRI is an independent risk factor for SCVS. SIRI = 3.63 × 109/L is the best cutoff value for diagnosing the occurrence of SCVS. When TC = 2.24 mmol/L and SIRI = 3.63 × 10%/L, its Youden Index is the largest (0.312, 0.296) and is the best cutoff value for predicting the occurrence of SCVS; at the same time, its prediction accuracy (area under the ROC curve (AUC)), sensitivity, specificity, the positive predictive value, and negative predictive value are 0.743, 72.70%, 80.10%, 77.53%, and 94.24% and 0.725, 70.60%, 76.90%, 73.49%, and 93.59%. Nomogram prediction model establishment and evaluation combined with the results of multifactor analysis are used to build an individual nomogram prediction model. The model has good prediction consistency (C-index = 0.685, P < 0.01). ROC analysis results showed that the model that combined SIRI and other standard variables (AUC = 0.896, 95% CI was 0.803-0.929, P < 0.001) was better than the model that did not combine SIRI (AUC = 0.859, 95% CI was 0.759-0.912, P < 0.001) and the model based only on SIRI (AUC = 0.725, 95% CI was 0.586-0.793, P = 0.001) has better predictive value for SCVS. Joint SIRI will optimize the prediction performance of the nomogram model and improve the early recognition and screening capabilities of SCVS.

Intravenous administration of dantrolene and nimodipine in combination significantly improves cerebral blood flow perfusion in a rat model of cerebral-induced vasospasm

Experimental evidence shows that concomitant administration of dantrolene and nimodipine has synergistic effects in reducing vasospasms in aortic rings from Sprague Dawley rats. To determine if this effect extends to the cerebral circulation, we investigated the effect of intravenous administration of dantrolene (2.5 mg/kg) and nimodipine (1 mg/kg and 2 mg/kg) on MCA blood flow velocity (BFV) in Sprague Dawley rats.

The effects of tacrolimus on cognitive functions in a rat model of cerebral vasospasm

The effects of tacrolimus on cognitive functions in a rat model of cerebral vasospasm

Computed tomography angiography findings predictive of post-intervention vasospasm in patients with aneurysmal subarachnoid hemorrhage.

To evaluate the association of CT/CT angiography (CTA) findings and clinical characteristics with subsequent vasospasm in patients with aneurysmal subarachnoid hemorrhage (aSAH). Consecutive presentation CTA head exams in patients with aSAH between January 2005 and June 2015 were retrospectively evaluated for intracranial arterial calcification, undulation and non-calcified stenosis. Additional variables including modified Fisher Scale (mFS), Glasgow Coma Scale (GCS) and neurological exam status were reviewed. Associations of CTA findings with the incidence of angiographic vasospasm were assessed with multivariate logistic regression models using the least absolute shrinkage and selection operator machine-learning algorithm. Model performance was summarized using c-index with bootstrap optimism-adjustment. Intracranial arterial calcification, seen in 51.7% of 195 total patients, was protective against vasospasm (OR-0.6; 95% CI-0.52-0.67; p = 0.009), while arterial undulation (24%) was associated with subsequent vasospasm (OR-2.6; 95% CI-1.3-5.1; p = 0.007). Non-calcified intracranial arterial stenosis (5%) was associated with subsequent vasospasm, (OR-4.7; 95% CI-1.0-22.8; p = 0.054). Least absolute shrinkage and selection operator selected all three CTA findings as predictors in a multivariate model for vasospasm in addition to clinical factors, which demonstrated superior predictive performance (c-index-0.74; 95% CI-0.69-0.82) compared to a model based on mFS and clinical factors only (c-index-0.66; 95% CI-0.57-0.75; p = 0.010 for the difference). Presentation CTA findings combined with clinical factors may better predict the development of vasospasm in patients with aSAH compared to current prognostic models alone. The combination of initial CT/CTA and clinical findings better predict development of vasospasm after aSAH. This can lead to better markers for use in future clinical trials to develop vasospasm preventative treatments and potentially provide better targets for early aggressive treatment.

The Effects of Ozone Oxidative Preconditioning on Subarachnoid Hemorrhage via Rat Cerebral Vasospasm Model

Objective: Cerebral vasospasm after subarachnoid hemorrhage (SAH) is a major cause of morbidity and mortality. Inflammation is the major molecular mechanism observed in vasospastic SAH. Ozone (O3) has been used as a therapeutic agent in the treatment of various conditions and diseases for years. The aim of this study was to evaluate the anti-inflammatory effect of ozone oxidative preconditioning (OOP) in a rat model of SAH in order to assess the therapeutic potential of O3 in SAH therapy. Materials and Methods: In the presented study, an experimental in vivo SAH rat model that provided constriction of large cerebral arteries was used. The inflammatory response of cerebral vasospasm after SAH and the effects of OOP were evaluated by comparing the mRNA levels of inflammatory molecules (tumor necrosis factor-α, interleukin-1β, and intercellular adhesion molecule-1) in the serum samples of rats. Results: The level of inflammatory molecules increased in vasospasm at 12 h, 24 h, and 48 h in the posttreatment groups. However, intraperitoneal OOP decreased the level of inflammatory molecules dramatically. Conclusions: Our study indicated that O3 treatment has potential in the management of inflammation created in a rat SAH model. These findings may inform further studies investigating possible uses of O3 in the treatment of vasospasm.

Sudden Cardiac Death in Anabolic-Androgenic Steroid Users: A Literature Review.

Background and objectives: Anabolic-androgenic steroids (AASs) are a group of synthetic molecules derived from testosterone and its related precursors. AASs are widely used illicitly by adolescents and athletes, especially by bodybuilders, both for aesthetic uses and as performance enhancers to increase muscle growth and lean body mass. When used illicitly they can damage health and cause disorders affecting several functions. Sudden cardiac death (SCD) is the most common medical cause of death in athletes. SCD in athletes has also been associated with the use of performance-enhancing drugs. This review aimed to focus on deaths related to AAS abuse to investigate the cardiac pathophysiological mechanism that underlies this type of death, which still needs to be fully investigated. Materials and Methods: This review was conducted using PubMed Central and Google Scholar databases, until 21 July 2020, using the following key terms: “((Sudden cardiac death) OR (Sudden death)) AND ((androgenic anabolic steroid) OR (androgenic anabolic steroids) OR (anabolic-androgenic steroids) OR (anabolic-androgenic steroid))”. Thirteen articles met the inclusion and exclusion criteria, for a total of 33 reported cases. Results: Of the 33 cases, 31 (93.9%) were males while only 2 (61%) were females. Mean age was 29.79 and, among sportsmen, the most represented sports activity was bodybuilding. In all cases there was a history of AAS abuse or a physical phenotype suggesting AAS use; the total usage period was unspecified in most cases. In 24 cases the results of the toxicological analysis were reported. The most detected AASs were nandrolone, testosterone, and stanozolol. The most frequently reported macroscopic alterations were cardiomegaly and left ventricular hypertrophy, while the histological alterations were foci of fibrosis and necrosis of the myocardial tissue. Conclusions: Four principal mechanisms responsible for SCD have been proposed in AAS abusers: the atherogenic model, the thrombosis model, the model of vasospasm induced by the release of nitric oxide, and the direct myocardial injury model. Hypertrophy, fibrosis, and necrosis represent a substrate for arrhythmias, especially when combined with exercise. Indeed, AAS use has been shown to change physiological cardiac remodeling of athletes to pathophysiological cardiac hypertrophy with an increased risk of life-threatening arrhythmias.

Assessment of sertraline activity in a vasospasm model following experimental subarachnoid haemorrhage

Vasospasm following subarachnoid haemorrhage (SAH) is a process yet to be fully clarified in terms of its aetiology and results. According to one of the many theories about vasospasm developing after SAH, the process results from an increase of pro-inflammatory agents and decrease in antioxidant agents. Other hand experimental studies on rats found a significant decrease in the pro-inflammatory parameters TNF-α and IL-1β in the blood values obtained after the use of sertraline. In this study, the findings regarding the effectiveness of sertraline in the treatment of vasospasm developing an experimental SAH model are presented. In this study, adult males of Spraque-Dawley breed, not used in any previous study and weighing between 250–350 g, were used. Rats were divided into 4 groups with the control group (n=5) and other groups (n=6 in each). Group 1 was the control, and Group 3 was the sertraline group. In Groups 2 and 4, SAH was initiated by giving rats autologous arterial blood in the cisterna magna. The tissues were examined in terms of mononuclear cell infiltration, vascular congestion, and neuron degeneration. In the experimental SAH model based on these values, it was found that the use of sertraline significantly reduced mononuclear cell infiltration, vascular congestion, and neuron degeneration. Moreover, in animal studies, it was shown that SSRIs increased neurogenesis and release of neurotrophins from the hippocampus. In our study, it was concluded that sertraline was effective in dissolving vasospasm in the experimental SAH model. However, we further believe that more experimental studies to investigate other SSRI compounds of the same family can contribute to the knowledge and understanding of this process.

Ameliorating the effects of Adalimumab on rabbits with experimental cerebral vasospasm after subarachnoid hemorrhage.

Adalimumab (ADA), which is a new-generation recombinant human monoclonal antibody for tumor necrosis factor α (TNFα), has strong anti-inflammatory effects. The role of enhanced inflammation is well established for the development and progression of cerebral vasospasm. Investigated in the present study is the probable ameliorating and neuroprotective effects of ADA in rabbits using a cerebral vasospasm model with biochemical and histopathological methods. Thirty male New-Zealand white rabbits were randomly divided into control, subarachnoid hemorrhage (SAH) only and SAH plus ADA treatment groups. SAH was established as a single cisterna magna autologous arterial blood injection. ADA treatment was started just after intracisternal blood injection and continued for 72 hours once a day. The animals were sacrificed 72 hours after the induction of SAH, serum and brainstem tissue obtained for investigations. Brainstem tissue and plasma levels of tumor necrosis factor-alpha and Interleukin-1β, brainstem tissue Matrix metalloproteinase-9 levels increased after SAH and partly decreased after treatment. Plasma levels of brain-derived neurotrophic factor decreased after SAH and partly restored after treatment. ADA treatment significantly increased the mean cross-sectional area of the vasospastic basilar arteries, reduced the basilar artery wall thickness and also ameliorates enhanced endothelial apoptosis. Findings obtained in this study suggest that ADA is an effective neuroprotective agent for ameliorating cerebral vasospasm in experimental rabbit vasospasm.

Protective Effects of Betanin against Oxidative Stress in a Peripheral Artery Vasospasm Model in Rat

Objective: The aim of this study is to determine protective/modulatory effects of betanin in a femoral artery vasospasm model in rats. Materials and Methods: Sprague-Dawley rats were divided into three groups. Group 1: sham (n = 7), group 2: vasospasm model only (n = 7), group 3: postoperative betanin treatment in the vasospasm model (n = 7). 100 mg/kg betanin was administered orally to group 3 for 7 days, postoperatively. Peripheral blood malondialdehyde (MDA) and nitric oxide (NO) levels were measured for the quantification of oxidative stress, lumen diameter and wall thickness of femoral artery segments were determined to assess vasodilator effects of betanin. Results: Femoral artery vasospasm formation significantly increased both MDA (13.54 ± 3.09 mmol/mL) and NO levels (0.61 ± 0.06 µmol/mL) relative to the sham (9.07 ± 1.09 and 0.48 ± 0.1, respectively). Upon betanin administration, both MDA and NO approached baseline levels (9.95 ± 0.92 and 0.5 ± 0.06, respectively). Pathological examination of lumen diameter and wall thickness of the femoral arteries also revealed that betanin administration resulted in significant increase in lumen diameter when compared to vasospasm group (614.15 ± 245.77 versus 117.40 ± 46.19 µm) and decrease in wall thickness (64.68 ± 14.13 versus 96.73 ± 9.20 µm). Conclusion: Betanin was shown to have protective effect against oxidative stress in a peripheral artery vasospasm model in rats. It may also have a role in mitigating maladaptive changes in arterial structure, as shown in pathological examination.

Effect of L-Arginine Therapy on Vasospasm: Experimental Study in Rats

Cerebral vasospasm occurring after subarachnoid hemorrhage is a serious cause of morbidity. Cerebral vasospasm-related studies aim to prevent complications after subarachnoid hemorrhage. Nitric oxide affects brain blood flow and local vascular hemodynamics. L-arginine is used in the synthesis of nitric oxide, and hence we have investigated the efficacy of L-arginine treatment by using femoral artery vasospasm model. Twenty-four male Sprague-Dawley rats have been divided into 3 groups as vasospasm, vasospasm+ L-arginine, and control. In this study, we have preferred the "Rat Femoral Artery Vasospasm Model" described by Okada etal. Rats in the vasospasm+ L-arginine group were given 300 mg/kg L-arginine for 7 days. At the end of the study, all samples of rat femoral arteries have been dissected and examined microscopically for histopathologic analysis. Statistical analysis was performed using Kruskal-Wallis and Mann-Whitney U tests, and P < 0.05 value was considered statistically significant. L-arginine treatment reduced the morphometric changes such as irregularity of the elastic lamina, disruption of the endothelial cells, vacuolization, and hemorrhages that are caused by vasospasm. When the wall thickness and lumen diameter measurements were evaluated statistically, significant improvement was observed in the vasospasm+ L-arginine group compared with the vasospasm group (P < 0.01). In our study, the use of L-arginine, as a nitric oxide substrate, improved the experimental vasospasm in rats. Therefore we think that L-arginine therapy can be used in the prevention and treatment of cerebral vasospasm after subarachnoid hemorrhage.

Effects of Intrathecal Verapamil on Cerebral Vasospasm in Experimental Rat Study

Verapamil, a calcium-channel blocker, has shown promising results on cerebral vasospasm. However, it has not yet been accepted for treatment or prevention purposes because of the associated side effects. Although the effective results of nimodipine and nicardipine's intrathecal administration are well known, intrathecal verapamil has not been considered earlier. We used an experimental subarachnoid hemorrhage-induced vasospasm model for the evaluation of vasodilator and neuroprotective effects of intrathecal verapamil. A total of 24 Sprague-Dawley rats were randomly divided into the following 3 groups: group 1 (sham), group 2 (subarachnoid hemorrhage), and group 3 (verapamil). A double hemorrhage method was used. Group 2 did not receive any treatment. Verapamil (Eporon, Dem Ilac, Turkey) at a dose of 1000 μg/kg was given intrathecally to group 3 rats. The animals were euthanized on day 7 of the procedure. Arterial wall thickness and lumen diameter in the basilar arterial cross-sectional areas, endothelin-1 serum level, oxidative stress index, and apoptosis were measured in all groups. In the verapamil group, wall thickness, endothelin-1 level, oxidative stress index, and apoptosis were found to be significantly lower than the subarachnoid hemorrhage group, but the lumen diameter was found to be greater. Intrathecal verapamil was found to decrease vasospasm parameters and apoptosis and increase the antioxidant and antiapoptotic pathways. Our findings suggest that intrathecal verapamil can prevent vasospasm, oxidative stress, and apoptosis after experimental subarachnoid hemorrhage.

A Comparative Analysis of the Effects of Melatonin and Nimodipine on Vasospasm

Objective: In this study, we aimed to compare the efficacy of nimodipine and melatonin in a rat femoral artery vasospasm model. Material and Methods: The rats were divided into five groups as follows: Group I (n=8): control group, Group II (n=8): vasospasm group, Group III (n=8): vasospasm + melatonin group, Group IV (n=8): vasospasm + nimodipine group, Group V (n=8 rats): vasospasm + melatonin + nimodipine group. At the end of the 7 th day, the femoral arteries were excised and histopathologically examined under light microscope. Results: Vascular wall of vasospasm group was relatively thicker when compared with the control group. There was a statistically significant difference between the wall thickness of Group II and Group III, IV and V. The maximum reduction of wall thickness was observed in Group V. There was no statistically significant difference in lumen diameter between Group I and Group IV. The lumen diameter was found to be increased in Group III, IV and V when compared with Group II. Conclusion: The development of experimental peripheral vasospasm has been reduced by the melatonin and nimodipine and their effect was increased when they were used concomitantly.

Morphometric Analysis of Dose-dependent Effect of Progesterone on Experimental Vasospasm-induced Rat Femoral Arteries.

Objective:Our aim of this study was to determine effective doses of progesterone which has a vasodilatory effect during the early stage of vasospasm. Cerebral vasospasm (CV) is a predominant cause of morbidity and mortality which develops following subarachnoidal hemorrhage (SAH). Etiopathogenesis of CV is multifactorial. Despite many previously performed studies on this issue, the mechanism by which blood and blood products in the subarachnoidal space induce CV has not been clarified yet.Materials and Methods:In our study, we used “Rat Femoral Artery Vasospasm Model” introduced by Okada et al. Thanks to easy procurement and maintenance of rats. Rats were divided into four groups as: Group 1 (n = 8; control group), Group 2 (n = 8; vasospasm group), Group 3 (n = 8; vasospasm + 3 mg/kg progesterone group), and Group 4 (n = 8; vasospasm +15 mg/kg progesterone group). Progesterone which is an endogenously synthesized natural steroid was preferred in our study. Progesterone increases the production of vasodilatory epoxyeicosatrienoic acid by acting on its binding sites termed as pregnane X receptor. It decreases the intracellular influx of Ca2+ by blocking the functioning of L-type channels in smooth muscle cells. It manifests another vasodilatory effect by decreasing expression of TxA2 receptor. In our study, at the end of the 7th day, where the most intense vasospasm is seen, 1 cm pieces were excised from the femoral arteries and histopathologically examined under light microscope.Results:Vascular walls of three vasospasm-induced groups were relatively thicker when compared with the control group. Drug-treated groups were not different from each other. Vascular walls of the groups treated with lower and higher doses of the drug were thinner when compared with the vasospasm group without any statistically significant difference between groups (P > 0.05). Luminal cross-sectional areas of the drug-treated groups did not differ from each other. Mean luminal cross-sectional areas of the control and the drug-treated groups were larger than that of the vasospasm group without any statistically significant intergroup difference (P > 0.05).Conclusion:Based on the results of our study, progesterone did not exert protective effects on vascular wall thickness, while histopathological examination of luminal cross-sectional areas revealed its vasodilatory effects without any statistically significant difference between groups. Starting from the study results obtained, we think that its potential use as a preventive agent against the development of post-SAH CV requires conduction of multicentered, placebo-controlled, randomized, and double-blind studies.

Establishment of modified "double injection of blood" subarachnoid hemorrhage induced delayed cerebral vasospasm model in rats

Objective The subarachnoid hemorrhage (SAH) models were established by modified injection of autologous blood into the rat cisterna magna and then assess the degree of delayed cerebral vasospasm. Methods The details of improved double injection of autologous blood is as folllows: (1) Stereotaxic apparatus was used to located the cisterna magna in the three-dimensional space. (2) Instead of manual injection, the micro-injection pump, which keep the volume and injection speed constant, was used. A total of 75 male SD rats were included in this study and randomly divided into the following three groups (n=25/group): sham group, control group and SAH group. SAH group, rats subjected to injection of autologous blood into the cisterna magna; control group, rats subjected to injection of the equal quantity saline; sham group, rats subjected to only explosion of atlanto-occipital membrane. The success rate and failure rate, neurological function, brain water content, changes of basilar artery, regional cerebral blood flow (rCBF) were observed. Results Neurological function in SAH group were significantly impaired as compared with sham group at day 1 (9.2±0.7 vs. 1.0±0.6, P=0.001). Brain water contents in SAH group were significantly increased as compared with sham group and control group at day1 [(79.98±0.11)% vs. (78.29±0.12)%, (78.39±0.13)%, P=0.001]. Hematoxylin and eosin (HE) staining results showed a significant reduce of basilar artery lumen diameter and area in SAH group than that in sham group at day5 [(325.200±15.156) μm vs. (461.000±22.705) μm, P=0.000; (80 739.200±7 297.735) μm2 vs. (167 124.200±7 067.155) μm2,P=0.000]. The result of rCBF of SAH group, measured by Laser speckle, also showed a significant decrease compared to sham group at day5 after SAH [(56.0±3.5)% vs. (97.2±1.7)%, (95.8±3.5)%, P=0.001]. Conclusion The stable and reliable subarachnoid hemorrhage model can be established by modified injection of autologous blood into the cisterna magna. Key words: Subarachnoid hemorrhage; Model; Cerebral vasospasm; Animal experimentation

An experimental rabbit model of symptomatic cerebral vasospasm with in vivo neuroimaging assessment and ex vivo histological validation.

Cerebral vasospasm (CVS) is a severe complication that occurs following aneurysmal subarachnoid hemorrhage (SAH). Magnetic resonance angiography (MRA) has been used to evaluate brain injury following SAH in humans. The present study was designed to assess a rabbit model of symptomatic CVS (SCVS) and the utility of MRA in evaluating SCVS in rabbits. Japanese white rabbits (n=24) were randomly divided into 2 equal groups: A sham group and a SAH group. Neurological scores were evaluated for 7 days following SAH. Basilar artery (BA) diameters were measured using MRA preoperatively and 7 days postoperatively. Rabbits were sacrificed 7 days following SAH and the BA diameter of each rabbit was determined using histological evaluation. Compared with the Sham group, neurological function was significantly reduced in the SAH group at all time points (P<0.05). Furthermore, the BA diameter was significantly smaller in the SAH group on day 7 compared with the baseline measurement (P<0.05). No significant difference was observed between histological and MRA findings in either group at day 7. Histological changes in the hippocampus consistent with ischemia were observed in the SAH group. Hippocampal ischemia was also identified in the SAH group via MRA and there was no difference in detection rates following the use of MRA and histochemistry. MRA appears to be an effective method for assessing vasospasms of the BA and ischemic changes to the hippocampus in a rabbit model of SCVS. Furthermore, the animal model used in the present study may be beneficial for the future study of SCVS.

Morphometric Analysis of the Effects of Manuka Honey on Vasospastic Femoral Arteries in Rats: An Experimental Study.

Objectives:The aim of this study was to determine if Manuka honey, a potent anti-inflammatory and antioxidant agent, had any effect on the development of vasospasm in an experimental subarachnoidal hemorrhage model constructed in rat femoral arteries.Methods:Twenty-four Wistar Albino strain rats were divided into 3 groups: Group 1 was the control group (n=8), Group 2 was the vasospasm group (n=8), and group 3 was the treatment group (n=8). The wall thickness (W) of the femoral arteries and the luminal diameter (L) were measured using morphometric methods. The data were analyzed with statistical software. The Mann-Whitney U-test was used to compare independent groups and Bonferroni post hoc analysis was used for multiple comparison tests. Significance for all of the results was established at p<0.05.Results:A statistically significant intergroup difference was detected in the mean L and W (p<0.001, p=0.001, respectively). The mean L value in Group 2 was statistically significantly less than that of Groups 1 and 3, while the mean W value was significantly greater (p<0.001 for all). However, no statistically significant difference was detected between Groups 1 and 3 with respect to the mean L and W values (p=0.064, p=0.954, respectively).Conclusion:Manuka honey exerts an antioxidant and anti-inflammatory effect via inhibition of inflammatory cytokines, including plasma tumor necrosis factor alpha, interleukin (IL)-1 beta, IL-6, and the lipid peroxidation level. This study statistically demonstrated that the anti-inflammatory and antioxidant properties of Manuka honey successfully inhibited the development of vasospasm in an experimentally induced vasospasm model in the femoral arteries of rats.