Changes In Basilar Artery Research Articles

Intimal Hemorrhage of Basilar Artery Induced by Severe Vasospasm Following Subarachnoid Hemorrhage: The Experimental Analysis.

Cerebral vasospasm, a serious complication of subarachnoid hemorrhage (SAH), has been extensively studied for its neurochemical and pathophysiologic mechanisms. However, the contribution of inner elastic membrane dissection and subintimal hemorrhage to basilar artery occlusion remains underexplored. This study investigates inner elastic membrane-related changes in the basilar artery after SAH. Twenty-four hybrid rabbits were divided into control, sham, and SAH groups, with SAH induced by autologous blood injection. After 2 weeks, basilar artery changes, vasospasm indexes (VSIs), and dissections were evaluated. The SAH group showed significantly higher VSI, with vascular wall thickening, luminal narrowing, convoluted smooth muscle cells, intimal elastic membrane disruption, endothelial cell desquamation, and apoptosis. Some SAH animals exhibited subintimal hemorrhage, inner elastic membrane dissection, and ruptures. Basilar arteries with subintimal hemorrhage had notably higher VSI. These findings highlight the role of subintimal hemorrhage and inner elastic membrane dissection in basilar artery occlusion post-SAH, offering valuable insights into vasospasm pathophysiology.

Effects of abnormal vertebral arteries and the circle of Willis on vertebrobasilar dolichoectasia: A multi-scale simulation study

BackgroundVertebrobasilar dolichoectasia is a rare cerebrovascular disease characterized by obvious extension, dilation and tortuosity of vertebrobasilar artery, and its pathophysiological mechanism is not clear. This study focused on local hemodynamic changes in basilar arteries with typical vertebrobasilar dolichoectasia, together with unbalanced vertebral arteries and abnormal structures of the circle of Willis, through multi-scale modeling. MethodsThree-dimensional models of 3 types of vertebrobasilar arteries were constructed from magnetic resonance images. The first type has no vertebrobasilar dolichoectasia, the second type has vertebrobasilar dolichoectasia and balanced vertebral arteries, and the third type has vertebrobasilar dolichoectasia and unbalanced vertebral arteries. A lumped parameter model of the circle of Willis was established and coupled to these three-dimensional models. FindingsThe results showed that unbalanced bilateral vertebral arteries, especially single vertebral artery deletion mutation, might associate with higher wall shear stress on anterior wall of basilar artery in patients with vertebrobasilar dolichoectasia. And unbalanced bilateral vertebral arteries would increase the blood pressure in basilar artery. Meanwhile, missing communicating arteries in the circle of Willis, especially bilateral posterior communicating arteries absences, would significantly increase blood pressure in basilar artery. The unilateral absence of posterior communicating arteries would increase differences in blood flow between the left and right posterior cerebral arteries. InterpretationThis study provided a multi-scale modeling method and some preliminary results for helping understand the role of hemodynamics in occurrence and development of vertebrobasilar dolichoectasia.

Role of ATP-sensitive potassium channels and inflammatory response of basilar artery smooth muscle cells in subarachnoid hemorrhage of rabbit and immune-modulation by shikonin

ObjectiveTo investigate the role of inflammatory response, oxidative damage and changes of ATP-sensitive potassium channels (sKATP) in basilar artery (BA) smooth muscle cells (SMCS) of rabbits in subarachnoid hemorrhage (SAH) model. MethodsTime course studies on inflammatory response by real-time PCR, oxidative process and function of isolated basilar artery after SAH in New Zealand White rabbits were performed. Basilar artery smooth muscle cells (BASMCs) in each group were obtained and whole-cell patch-clamp technique was applied to record cell membrane capacitance and KATP currents. The morphologies of basal arteries were analyzed. Protective effect of shikonin were also determine by same parameters. ResultsInflammatory cytokines levels were highest at 24h compare to 72h after SAH whereas the oxidative damage and cell death marker were at highest peak at 72h. Oxidative damage peak coincided with significant alterations in cell membrane capacitance, KATP currents and morphological changes in basilar arteries. Shikokin pretreatment attenuated early inflammatory response at 24h and associated oxidative damage at 72h. Finally, shikonin attenuated morphological changes in basilar arteries and dysfunction. ConclusionCurrents of ATP-sensitive potassium channels in basilar smooth muscle cells decreased after SAH by putative oxidative modification from immediate inflammatory response and can be protected by shikonin pretreatment.

Anti-apoptotic effect of Astragaloside IV on delayed cerebral vasospasm following subarachnoid hemorrhage in rats

Objective Investigate the effect of Astragaloside Ⅳ (AS-Ⅳ) on delayed cerebral vasospasm (DCVS) following subarachnoid hemorrhage. Methods The male SD rats were divided into Sham group (A), SAH+ AS-Ⅳ group (B), SAH model group (C) and SAH+ vehicle group (D). The model of DCVS following subarachnoid hemorrhage was made by the double injection method of occipital cistern. During the 5 days after model success, rats in the B group were treated with daily AS-Ⅳ (20 mg/kg) which was dissolved in 5% alcohol; rats in the D group were injected with identical volume of physiological saline containing 5% alcohol; rats in the SAH group and the Sham group were inject with identical volume of physiological saline. Morphological changes of basilar artery was observed by hematoxylin and eosin (HE) staining. The apoptosis of basilar artery endothelial cells and vascular smooth muscle cells was detected by terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL) staining. The cleaved cysteinyl aspartate-specific protease (Caspase)-3 expression in basilar artery was detected by immunohistochemical staining. The expression of B cell lymphoma/leukemia-2 (bcl-2), bcl-2 associated X protein (bax) and cleaved Caspase-3 was detected by Western blotting. Results Compared with Sham group, the basilar artery wall became thicker and lumen cross-sectional area became smaller. The expression of bax and cleaved Caspase-3 (P<0.05) was decreased in basilar artery (P<0.05). Compared with SAH+ vehicle group and SAH group, the expression of cleaved Caspase-3 in SAH+ AS-Ⅳ group increased (P<0.05) and the expression of bax and cleaved Caspase-3 decreased after AS-Ⅳ intervention (Cleaved Caspase-3: 0.030 8±0.003 2 vs. 0.070 4±0.006 0, 0.069 0±0.005 7, P<0.05). Conclusion AS-Ⅳ can relieve delayed cerebral vasospasm and its mechanism may be related to the fact that AS-Ⅳ can interfere with the apoptosis signaling pathway mediated by bcl-2, bax and Caspase-3. Key words: Astragaloside Ⅳ; Subarachnoid hemorrhage; Delayed cerebral vasospasm; Apoptosis

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

Basilar Artery Changes in Fabry Disease.

Dolichoectasia of the basilar artery is a characteristic finding of Fabry disease. However, its prevalence, severity, and course have been poorly studied. This study quantitatively evaluated, by MRA, a panel of basilar artery parameters in a large cohort of patients with Fabry disease. Basilar artery mean diameter, curved length, "origin-to-end" linear distance (linear length), and tortuosity index ([curved length ÷ linear length] - 1) were retrospectively measured on 1.5T MRA studies of 110 patients with Fabry disease (mean age, 39.4 ± 18.6 years; 40 males) and 108 control patients (mean age, 42.0 ± 18.2 years; 40 males). Patients with Fabry disease had increased basilar artery mean diameter (P < .001) and basilar artery linear length (P = .02) compared with control patients. Basilar artery curved length and tortuosity index correlated with age in both groups (P < .001), whereas basilar artery linear length correlated with age only in patients with Fabry disease (P = .002). Patients with Fabry disease showed a basilar artery curved length mean increase of 4.2% (9.7% in male patients with Fabry disease versus male control patients), whereas the basilar artery mean diameter had a mean increase of 12.4% (14.3% in male patients with Fabry disease versus male control patients). Male patients with Fabry disease had increased basilar artery mean diameter, curved length, and tortuosity index compared with female patients with Fabry disease (P = .04, P = .02, and P < .001, respectively) and male control patients (P < .001, P = .01, and P = .006, respectively). Female patients with Fabry disease demonstrated an age-dependent increase of basilar artery mean diameter that became significant (P < .001) compared with female control patients above the age of 45 years. The basilar artery of patients with FD is subjected to major remodeling that differs according to age and sex, thus providing interesting clues about the pathophysiology of cerebral vessels in Fabry disease.

Early morphology and pathology of the basilar artery remodeling induced by hemodynamic changes

Objective To explore the basilar artery morphology and pathology after hemodynamic changes of basilar artery. Methods New Zealand white rabbits were subjected to bilateral common carotid artery ligation to produce compensatory vertebrobasilar artery flow increase. The basilar artery flow velocity was monitored by transcranial Doppler before the procedure and at 1 day, 1 week and 2 weeks after the procedure. DSA was performed at 1 week and 2 weeks after the procedure respectively and the basilar artery diameter and the extent of tortuosity were measured. The basilar artery tissues were harvested at 1 week and 2 weeks after the procedure and examined histologically by EVG and Masson staining. Results The basilar artery flow velocity of New Zealand white rabbit was increased significantly subjected to common carotid artery ligation (10.99 ml/min vs 36.53 ml/min, P<0.001). One or two weeks after surgery, the basilar artery diameter was expanded (0.60 mm vs 0.82 mm; 0.73 mm vs 1.03 mm, P<0.001), and the artery was curved. The internal elastic layer of artery was intact with smooth muscle cells proliferation in response to high flow and shear stress. The basilar artery was bent to the left side in 57.1% of all rabbits and there was significant difference compared with that of preoperation. Conclusions The hemodynamic increasing of the basilar artery after bilateral common carotid artery ligation of New Zealand white rabbits resulted in expansion and tortuosity of the basilar artery. Key words: Basilar artery; Hemodynamic; Vascular remodeling; Angiography

Moving Vessel Wall Research Beyond the Plaque

The overlap between atherosclerotic disease of the cerebrovascular, cardiovascular, and peripheral vasculature has long been recognized. Carotid atherosclerosis increases the odds of coronary events1 and of finding atherosclerotic changes in coronary, cerebral, aortic, and iliac arteries.2 Similarly, peripheral vascular disease is a risk factor for both stroke and myocardial infarction and is associated with extracranial carotid and intracranial atherosclerosis.3,4 Data from the Reduction of Atherothrombosis for Continued Health (REACH) registry show that atherosclerosis in 1 vascular bed increases the risk of adverse outcomes in each of the other locations, and that multiple disease locations at baseline increase the risk of subsequent cardiovascular and cerebrovascular events.5 Given shared underlying risk factors and pathophysiology, it is not surprising that those who present with atherosclerotic disease in 1 vascular bed are at increased risk for disease in others.6 See accompanying article on page 2240 It is fair to say that although considerable attention has been given to atherosclerotic disease affecting peripheral, cardiac, and carotid arteries, important gaps remain in our knowledge. For example, the intracranial circulation has received comparatively …

Simvastatin attenuated cerebrovascular cell proliferation in the development of hypertension through Rho/Rho-kinase pathway.

The cerebrovascular remodeling is a prominent feature of hypertension and considered as a major risk of stroke. Statins may suppress the activation of the Rho/Rho-kinase pathway and have pleiotropic actions against the development of vascular remodeling. We hypothesized that the inhibition of the Rho/Rho-kinase pathway by simvastatin during hypertension could recuperate the pathological changes of basilar artery through the downregulation of cell proliferation. To resolve the problem, we used 2-kid, 2-clip rat as a hypertension model and evaluated the effect of simvastatin on the Rho/Rho-kinase pathway. In addition, we assessed the changes of the proliferation rate by CCK-8 assay in basilar artery smooth muscle cells. Our results from this study showed that a continuous increase in the plasma endothelin-1 (ET-1) concentration and the Rho/Rho-kinase activity was positively correlated with changes in blood pressure in the hypertensive rat. Simvastatin ameliorated the upregulated Rho/Rho-kinase activity and cell proliferation during hypertension. Moreover, simvastatin, the RhoA inhibitor C3, and the RhoA-kinase inhibitor Y27632 all attenuated the proliferation rate induced by ET-1 in basilar artery smooth muscle cells via the Rho/Rho-kinase signaling pathway. In conclusion, simvastatin attenuated ET-1-induced proliferation through the Rho/Rho-kinase signaling pathway in hypertensive rat basilar artery, and it may be an excellent reagent to protect vascular remodeling and stroke.

Effects of nimodipine on rabbits with symptomatic cerebral vasospasm

To investigate the effects of nimodipine on symptomatic cerebral vasospasm in rabbits. Twenty four japanese white rabbits which ligation of bilateral common carotid arteries and no neurological deficits were randomized to sham-operation, subarachnoid hemorrhage (SAH) and nimodipine which injected of nimodipine 0.1 mg/kg, continuous vein administration 5 day. The behavior scores, neurological scores were observed everyday and cerebral angiography changes were measured twice by 3D-CTA, and basilar artery was removed for pathological examination after last CTA examination. In SAH group, The basilar artery were significantly vasoconstrictive on 5 days, neurological scores were increased, and the basilar artery was found apoptosis-like changes under light microscopic and electron microscope. Nimodipine group could not dilated the basilar artery arteriospasm after SAH, but it could attenuate neurological deficit, and obviously alleviate the pathological changes of basilar artery. Nimodipine could not vasodilation of basilar artery in SCVS, but obviously could alleviate neurological changes and pathological changes of basilar artery in rabbits with symptomatic cerebral vasospasm.

Effects of human tissue kallikrein on cerebral vasospasm: experiment with rabbits

To study the effects of human tissue kallikrein (HTK) on symptomatic cerebral vasospasm (CVS) after subarachnoid hemorrhage (SAH). Forty rabbits underwent occlusion of bilateral carotid. Two weeks later the 28 surviving rabbits were randomly divided into to 4 groups: shamed-operation group (n = 8) undergoing injection of normal saline into the cisterna magna on day 1 and day 3, SAH group (n = 6) undergoing injection of nonheparinized autologous arterial blood into the cisterna magna, HTK therapy group (n = 6) undergoing blood injection into the cisterna magna and then injection of HTK via ear marginal vein daily for 3 days, and nimodipine (ND) therapy group (n = 6) undergoing blood injection into the cisterna magna and then injection of ND via ear marginal vein. 3-dimension-CT angiography (3-D CTA) was used to measure the basilar artery diameter on D(0) and D(5). On D(6) the rabbits were killed with their basilar arteries taken out to undergo light microscopic examination. Blood could be seen in the basis cephalic of the 3 groups undergoing blood injection. 3-D CTA showed that arteriospasm was seen in the SAH and ND groups but not in the HTK group. Microscopy showed obvious pathological changes in basilar artery in the SAH and ND groups but not in the HTK group. HTK given early after SAH effectively alleviates the symptomatic cerebral vasospasm.

The effect of ecdysterone on cerebral vasospasm following experimental subarachnoid hemorrhage in vitro and in vivo

Objectives: Cerebral vasospasm has been the dreaded complication of ruptured intracranial aneurysms. Worldwide effort has led to many promising experimental treatments but none was confirmed to be effective in clinical trials. Ecdysterone is an insect steroid hormone. Our previous study showed that ecdysterone might prevent cerebral vasospasm in vitro. Even after all these works, rare attempts have been made to test the effect of ecdysterone on vascular adventitial fibroblast (VAF) proliferation, a process known to play an important role in various pathogenic vascular conditions. Thus, we tested the hypothesis that ecdysterone could affect VAF characteristics and have an effect on SAH induced cerebral vasospasm.Methods: OxyHb of 100 μM was used in the in vitro study to mimic the clinical situation. The effect of OxyHb on the cell proliferation and migration of cultured aortic smooth muscle cells was investigated. In the in vivo study, 20 rabbits were equally divided into four groups: control group, SAH group, SAH/nimodipine group and SAH/ecdysterone group. Changes in neurological function and cerebral angiograms were observed after SAH.Results: OxyHb increased the proliferation of vascular adventitial fibroblasts at 24 hours. Ecdysterone co-treatment was apparently similar to the suppression of proliferation. Cell cycle analysis indicated that ecdysterone inhibited the progression of vascular adventitial fibroblasts from G1 to S. The results of the migration assay showed that 100 μM OxyHb obviously prompted vascular adventitial fibroblast migration and that ecdysterone would attenuate this effect. In the SAH/nimodipine and SAH/ecdysterone groups, neurological deficit, cerebral vasospasm and structural changes in basilar artery were alleviated with nimodipine or ecdysterone treatment.Conclusion: Ecdysterone could affect vascular adventitial fibroblast characteristics and attenuate vasospasm after SAH.

Collagen network changes in basilar artery in aging

The aim of this study was to examine and evaluate morphometrically age-related changes in collagen network in the tunica media of human basilar artery. Histological analysis of the basilar arteries obtained from 89 individuals, aged 20 to 85 years, was performed. The study has been carried out by standard histological technique; histological samples were stained with picrosirius red. Detailed quantitative analysis of collagen bundle network in the tunica media of basilar artery was performed. We analyzed collagen network area, perimeter and number of collagen bundles in the tunica media of the basilar artery. After investigation of age-related changes in collagen network area in men and women, we determined that in both genders collagen network area in the tunica media of the basilar artery increased with age. Analyzing the perimeter and number of collagen bundles in both genders by different age groups, it was found that they decreased with age. We found a statistically significant correlation between all the measured parameters and the age. The area of collagen bundles increased, the number and perimeter of collagen bundles decreased with age in both genders in the tunica media of human basilar artery. While aging, the structure of collagen bundle network became less branchy, collagen fibers merged, their cross section area enlarged.

Prevention and reversal of vasospasm and ultrastructural changes in basilar artery by continuous infusion of CGS 35066 following subarachnoid hemorrhage.

Endothelin-1, a potent vasoconstrictive peptide, has been implicated in the pathogenesis of cerebral vasospasm following subarachnoid hemorrhage (SAH). The goal of this study was to evaluate the effect of continuous intravenous infusion of a highly selective endothelin-converting enzyme-1 inhibitor, CGS 35066, on the prevention and reversal of cerebral vasospasm following SAH. New Zealand white rabbits were subjected to SAH by injecting autologous arterial blood into the cisterna magna. Infusion of CGS 35066 at dosages of 1, 3, or 10 mg/kg/ day was initiated either 1 hr and 24 hrs later in the prevention and reversal protocols, respectively. Animals were sacrificed by perfusion-fixation 48 hrs after SAH induction. The cross-sectional areas of basilar arteries were measured using computer-assisted videomicroscopy. Ultrastructural changes in basilar arteries were determined using electron microscopy. CGS 35066 significantly prevented and reversed the arterial narrowing after SAH in all three groups. The mean cross-sectional areas of arteries from animals in both the prevention and reversal protocol groups that received 10 mg/kg/day of CGS 35066 did not differ significantly from those of the healthy controls. Histological studies of the basilar artery in the 10 mg/kg/day treatment group did not show pathomorphological changes, such as corrugation of the endothelium seen at 2 days after SAH induction or vacuole formation in the endothelial cells noted in the vehicle-treated SAH group. These findings suggest that CGS 35066 is a promising therapeutic agent for the prevention and reversal of cerebral vasospasm after SAH. It also prevents the pathological changes in vascular walls due to SAH.