Vascular corrosion casts mirroring early morphological changes that lead to the formation of saccular cerebral aneurysm: an experimental study in rats

2005 ◽  
Vol 102 (3) ◽  
pp. 532-535 ◽  
Author(s):  
Mohammad A. Jamous ◽  
Shinji Nagahiro ◽  
Keiko T. Kitazato ◽  
Koichi Satoh ◽  
Junichiro Satomi
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Endothelial Cell ◽  
Cerebral Aneurysm ◽  
Morphological Changes ◽  
Cerebral Aneurysms ◽  
Content Type ◽  
Aneurysmal Dilation ◽  
Hemodynamic Shear Stress ◽  
Fine Print

Object. The formation of cerebral aneurysms involves complex processes and little is known about the mechanisms by which they originate, grow, and rupture. The purpose of this study was to identify early ultrastructural morphological changes that lead to the formation of experimental cerebral aneurysms. Methods. Twenty male Sprague—Dawley rats were subjected to cerebral aneurysm induction (renal hypertension and right common carotid artery ligation); 10 intact rats served as the control group. The animals were killed after 2 months, and a vascular corrosion cast of their cerebral arteries was prepared and screened for aneurysm development by using a scanning electron microscope. Sequential morphological changes observed at the cerebral artery bifurcation in response to hemodynamic shear stress included endothelial changes, intimal pad elevation, and saccular dilation. Endothelial cell changes were the first observed morphological changes; they were followed by various degrees of artery wall dilation. No aneurysmal changes developed in any of the control rats. Of the 20 surgically treated rats, 11 displayed aneurysmal changes. In five of these animals only changes in the endothelial cell imprints could be identified. In the other six rats morphological changes in endothelial cells were associated with different stages of aneurysmal dilation. Conclusions. This is the first study to demonstrate in vivo early morphological changes that lead to the formation of cerebral aneurysms. The morphological findings indicate the principal role of endothelial cells in the pathogenesis of cerebral aneurysms and suggest that hemodynamic shear stress and blood flow patterns may precipitate these early changes.

Evidence for telomerase involvement in the angiogenesis of astrocytic tumors: expression of human telomerase reverse transcriptase messenger RNA by vascular endothelial cells

2001 ◽  
Vol 94 (6) ◽  
pp. 961-971 ◽  
Author(s):  
Roberto Pallini ◽  
Francesco Pierconti ◽  
Maria Laura Falchetti ◽  
Daniela D'Arcangelo ◽  
Eduardo Fernandez ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Endothelial Cell Proliferation ◽  
Vascular Endothelial ◽  
Astrocytic Tumors ◽  
Htert Mrna ◽  
Content Type ◽  
Human Telomerase ◽  
Fine Print

Object. Evidence from recent in vitro studies indicates that reactivation of telomerase, the enzyme that synthesizes the telomere ends of chromosomes, is a crucial event in the unlimited clonal expansion of endothelial cells that precedes the neoplastic conversion of these cells. It is known that high-grade gliomas express telomerase and that, in these neoplasms, proliferating endothelial cells may undergo transformational changes with development of sarcomatous components within the primitive tumor. To assess whether telomerase is involved in the endothelial cell proliferation that characterizes brain tumor angiogenesis, the authors investigated at the single-cell level the expression of messenger (m)RNA for the human telomerase catalytic subunit human telomerase reverse transcriptase (hTERT) by vascular cells of astrocytic tumors. Methods. The in situ hybridization (ISH) method was performed by processing histological sections with specific riboprobes for hTERT and for c-myc, an oncogene that is known to upregulate hTERT. Results of the ISH studies were compared with proliferative activity, as estimated by Ki-67 immunostaining. The expression of hTERT mRNA by vascular endothelial cells was related to the histological grade of the tumor because it was detected in five (29%) of 17 low-grade astrocytomas, nine (56%) of 16 anaplastic astrocytomas, and 19 (100%) of 19 glioblastomas multiforme (GBMs). Expression of c-myc mRNA was strictly correlated with that of hTERT mRNA. In low-grade astrocytomas and anaplastic astrocytomas, a dissociation was noted between hTERT mRNA expression and the proliferation rate of endothelial cells. Conversely, GBMs displayed a significant correlation between the level of hTERT mRNA expression and endothelial cell proliferation. Data from an in vitro assay in which human umbilical vein endothelial cells were stimulated to proliferate by adding vascular endothelial growth factor and an ISH study of newly formed vessels surrounding brain infarcts confirmed that expression of hTERT mRNA does not merely reflect the proliferative status of endothelial cells but represents a specific feature of brain tumor neovascularization. Conclusions. The results of this study are consistent with a role of telomerase in the angiogenesis of astrocytic tumors. Expression of hTERT mRNA by tumor vascular cells is an early event during the progression of astrocytic tumors, which precedes endothelial cell proliferation and may represent a first sign of dedifferentiation. Other than elucidating the mechanisms of tumor angiogenesis, these results encourage research on antitelomerase drugs for the treatment of malignant gliomas.

Antegrade recanalization of a completely embolized vertebral artery after endovascular treatment of a ruptured intracranial dissecting aneurysm

2005 ◽  
Vol 102 (1) ◽  
pp. 161-166 ◽  
Author(s):  
Motoshi Sawada ◽  
Yasuhiko Kaku ◽  
Shinichi Yoshimura ◽  
Masahiro Kawaguchi ◽  
Takashi Matsuhisa ◽  
...  
Keyword(s):  
Vertebral Artery ◽  
Cerebral Aneurysms ◽  
Systemic Circulation ◽  
Parent Artery ◽  
Content Type ◽  
Endovascular Occlusion ◽  
Aneurysmal Dilation ◽  
Dissecting Aneurysms ◽  
Fine Print

✓ Occlusion of the parent artery is a traditional method of treatment of unclippable cerebral aneurysms. Surgical or endovascular occlusion of the parent artery proximal to the aneurysm has been recommended for the treatment of dissecting aneurysms located in the vertebrobasilar circulation. Nevertheless, occlusion of the parent artery may not result in permanent exclusion of the aneurysm from the systemic circulation because, occasionally, postoperative rebleeding occurs after proximal occlusion. Alternatively, endovascular occlusion of the affected site, including the aneurysmal dilation, and parent artery, is a safe and reliable treatment for dissecting aneurysms. The authors present two rare cases of ruptured vertebral artery (VA) dissecting aneurysms that were treated by endovascular occlusion of the affected site including the aneurysm and parent artery by using Guglielmi detachable coils. In both cases the VA recanalized in an antegrade fashion during the follow-up period. Based on these unique cases, the authors suggest that a careful angiographic follow up of dissecting aneurysms is required, even in patients successfully treated with endovascular occlusion of the affected artery and aneurysm.

Endothelial Cell Morphologic Response to Asymmetric Stenosis Hemodynamics: Effects of Spatial Wall Shear Stress Gradients

2010 ◽  
Vol 132 (8) ◽  
Author(s):  
Leonie Rouleau ◽  
Monica Farcas ◽  
Jean-Claude Tardif ◽  
Rosaire Mongrain ◽  
Richard L. Leask
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Endothelial Cell ◽  
Wall Shear Stress ◽  
Atherosclerotic Plaque ◽  
Morphological Changes ◽  
Stress Gradients ◽  
Spatial Gradients ◽  
Wall Shear

Endothelial cells are known to respond to hemodynamic forces. Their phenotype has been suggested to differ between atheroprone and atheroprotective regions of the vasculature, which are characterized by the local hemodynamic environment. Once an atherosclerotic plaque has formed in a vessel, the obstruction creates complex spatial gradients in wall shear stress. Endothelial cell response to wall shear stress may be linked to the stability of coronary plaques. Unfortunately, in vitro studies of the endothelial cell involvement in plaque stability have been limited by unrealistic and simplified geometries, which cannot reproduce accurately the hemodynamics created by a coronary stenosis. Hence, in an attempt to better replicate the spatial wall shear stress gradient patterns in an atherosclerotic region, a three dimensional asymmetric stenosis model was created. Human abdominal aortic endothelial cells were exposed to steady flow (Re=50, 100, and 200 and τ=4.5 dyn/cm2, 9 dyn/cm2, and 18 dyn/cm2) in idealized 50% asymmetric stenosis and straight/tubular in vitro models. Local morphological changes that occur due to magnitude, duration, and spatial gradients were quantified to identify differences in cell response. In the one dimensional flow regions, where flow is fully developed and uniform wall shear stress is observed, cells aligned in flow direction and had a spindlelike shape when compared with static controls. Morphological changes were progressive and a function of time and magnitude in these regions. Cells were more randomly oriented and had a more cobblestone shape in regions of spatial wall shear stress gradients. These regions were present, both proximal and distal, at the stenosis and on the wall opposite to the stenosis. The response of endothelial cells to spatial wall shear stress gradients both in regions of acceleration and deceleration and without flow recirculation has not been previously reported. This study shows the dependence of endothelial cell morphology on spatial wall shear stress gradients and demonstrates that care must be taken to account for altered phenotype due to geometric features. These results may help explain plaque stability, as cells in shoulder regions near an atherosclerotic plaque had a cobblestone morphology indicating that they may be more permeable to subendothelial transport and express prothrombotic factors, which would increase the risk of atherothrombosis.

Nonvisualization of a large cerebral aneurysm despite highresolution magnetic resonance angiography

1995 ◽  
Vol 82 (2) ◽  
pp. 294-295 ◽  
Author(s):  
Alan Turtz ◽  
David Allen ◽  
Robert Koenigsberg ◽  
H. Warren Goldman
Keyword(s):  
Magnetic Resonance ◽  
High Resolution ◽  
Magnetic Resonance Angiography ◽  
Cerebral Aneurysm ◽  
Mr Angiography ◽  
Cerebral Aneurysms ◽  
Arterial Aneurysm ◽  
Content Type ◽  
Fine Print

✓ The use of magnetic resonance (MR) angiography as a safe, accurate, and reliable substitute for invasive cerebral arteriography has been anticipated as refinements in this technique are introduced. We present the case of an unruptured, 11-mm pericallosal arterial aneurysm not visualized on high-resolution MR angiography. Although this case may be atypical, we caution against complete reliance on this test for exclusion of the presence of cerebral aneurysms.

Outcomes after cerebral aneurysm clip occlusion in the United States: the need for evidence-based hospital referral

2003 ◽  
Vol 99 (6) ◽  
pp. 947-952 ◽  
Author(s):  
John A. Cowan ◽  
Justin B. Dimick ◽  
Reid M. Wainess ◽  
Gilbert R. Upchurch ◽  
B. Gregory Thompson
Keyword(s):  
Cerebral Aneurysm ◽  
Cerebral Aneurysms ◽  
High Volume ◽  
Evidence Based ◽  
Content Type ◽  
Aneurysm Clip ◽  
Low Volume ◽  
Clip Occlusion ◽  
Very High ◽  
Fine Print

Object. In an age of multimodality and multidisciplinary treatment of cerebral aneurysms, patient outcomes have improved significantly. For a number of complex surgical procedures, hospitals with high case volumes yield superior outcomes. The effect of hospital volume on the mortality rate after emergency and elective cerebral aneurysm clip occlusion in a nationally representative sample of patients is unknown. Methods. Using clinical data derived from the Nationwide Inpatient Sample for the years from 1995 through 1999, 12,023 patients who underwent clip occlusion of a cerebral aneurysm (International Classification of Diseases, Ninth Revision, Clinical Modification code 3951) were included. Patient age, comorbid conditions, nature of admission, and diagnosis of subarachnoid hemorrhage were abstracted. Hospital case volume was grouped into quartiles. Unadjusted and case-mix adjusted analyses were performed. The mean patient age was 53.2 ± 13.5 years. The overall crude postoperative mortality rates for emergency and elective aneurysm clip occlusion were 12.2 and 6.6%, respectively. Very low volume hospitals demonstrated higher mortality rates than very high volume hospitals for both emergency (14.7 compared with 8.9%, p < 0.001) and elective (9.4 compared with 4.5%, p < 0.001) aneurysm surgery. Patient-specific predictors of death in the multivariate model were renal disease (odds ratio [OR] 3.32, p < 0.042); age (> 60 years, OR 2.36, p < 0.001; 51–60 years, OR 1.63, p < 0.001; 40–50 years, OR 1.25, p = 0.047); chronic obstructive pulmonary disease (present, OR 1.52, p < 0.001); and nature of admission (emergency, OR 1.18, p = 0.03). Provider-specific predictors of death included very low volume (OR 1.59, p < 0.001); low-volume (OR 1.37, p = 0.001); and high-volume (OR 1.45, p < 0.001) hospitals compared with very high volume hospitals. Conclusions. A significant volume—outcome effect exists for surgical treatment of cerebral aneurysms in the US. Factors influencing this effect should be investigated to guide future healthcare policy and evidence-based referral. Whenever possible, healthcare practitioners should refer patients to centers in which superior outcomes are consistently demonstrated.

Ultrastructural observations of the capsule of chronic subdural hematoma in various clinical stages

1975 ◽  
Vol 43 (5) ◽  
pp. 569-578 ◽  
Author(s):  
So Sato ◽  
Jiro Suzuki
Keyword(s):  
Endothelial Cells ◽  
Subdural Hematoma ◽  
Morphological Changes ◽  
Chronic Subdural Hematoma ◽  
Neurological Deficits ◽  
High Permeability ◽  
Content Type ◽  
Clinical Stages ◽  
Capillary Endothelial Cells ◽  
Fine Print

✓ The authors used light and electron microscope to examine the capsules of chronic subdural hematoma in 33 cases. In cases with neurological deficits, capillary endothelial cells in the capsule had many cytoplasmic protrusions and fenestrations, suggesting high permeability of the capillary wall. Endothelial degeneration was also observed in these cases. These morphological changes were reversed by osmotherapy. Formation of collagen fibrils from fibroblasts in the hematoma capsule was frequently observed in the cases treated by osmotherapy.

Flow changes caused by the sequential placement of stents across the neck of sidewall cerebral aneurysms

2005 ◽  
Vol 103 (5) ◽  
pp. 891-902 ◽  
Author(s):  
Gádor Cantón ◽  
David I. Levy ◽  
Juan C. Lasheras ◽  
Peter K. Nelson
Keyword(s):  
Shear Stress ◽  
Velocity Field ◽  
Cerebral Aneurysms ◽  
Parent Artery ◽  
Shear Stresses ◽  
Content Type ◽  
Aneurysm Neck ◽  
Aneurysm Wall ◽  
Aneurysm Model ◽  
Fine Print

Object. The goal of this study was to quantify the reduction in velocity, vorticity, and shear stresses resulting from the sequential placement of stents across the neck of sidewall cerebral aneurysms. Methods. A digital particle image velocimetry (DPIV) system was used to measure the pulsatile velocity field within a flexible silicone sidewall intracranial aneurysm model and at the aneurysm neck–parent artery interface in this model. The DPIV system is capable of providing an instantaneous, quantitative two-dimensional measurement of the velocity vector field of “blood” flow inside the aneurysm pouch and the parent vessel, and its changes at varying stages of the cardiac cycle. The corresponding vorticity and shear stress fields are then computed from the velocity field data. Three Neuroform stents (Boston Scientific/Target), each with a strut thickness between 60 and 65 µm, were subsequently placed across the neck of the aneurysm model and measurements were obtained after each stent had been placed. The authors measured a consistent decrease in the values of the maximal averaged velocity, vorticity, and shear stress after placing one, two, and three stents. Measurements of the circulation inside the sac demonstrated a systematic reduction in the strength of the vortex due to the stent placement. The decrease in the magnitude of the aforementioned quantities after the first stent was placed was remarkable. Placement of two or three stents led to a less significant reduction than placement of the first stent. Conclusions. The use of multiple flexible intravascular stents effectively reduces the strength of the vortex forming in an aneurysm sac and results in a decrease in the magnitude of stresses acting on the aneurysm wall.

Vascular ultrastructure in human meningiomas and schwannomas

1973 ◽  
Vol 38 (4) ◽  
pp. 409-419 ◽  
Author(s):  
Don M. Long
Keyword(s):  
Electron Microscopy ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Fluorescence Microscopy ◽  
Cell Junctions ◽  
Content Type ◽  
Cerebrovascular Permeability ◽  
Human Meningiomas ◽  
Fine Print

✓ Nineteen meningiomas and schwannomas have been studied by fluorescence microscopy and electron microscopy. Increased cerebrovascular permeability to protein was demonstrated in each tumor. The anatomical explanation for this increased permeability to protein was found in open endothelial cell junctions, gaps between endothelial cells, and fenestrations in capillary endothelial membranes.

Clinicopathological study of cerebral aneurysms

1978 ◽  
Vol 48 (4) ◽  
pp. 505-514 ◽  
Author(s):  
Jiro Suzuki ◽  
Hiro Ohara
Keyword(s):  
Endothelial Cells ◽  
Blood Flow ◽  
Cerebrospinal Fluid ◽  
Cerebral Arteries ◽  
Fibrous Tissue ◽  
Cerebral Aneurysms ◽  
Content Type ◽  
Clinicopathological Study ◽  
The Media ◽  
Fine Print

✓ The origin and mechanism of rupture, repair, and growth of intracranial saccular aneurysms are reported in an investigation of 45 aneurysms (23 unruptured and 22 ruptured) found in 34 brain specimens. Gaps in the media at the bifurcations of cerebral arteries are important for aneurysmal formation. The walls of aneurysms smaller than 3 mm in diameter are mainly composed of endothelial cells, and fibrous tissue. When aneurysms grow larger than 4 mm, the walls become collagenous and extremely thin portions develop in their domes, forming potential rupture points. Immediately after the rupture, bleeding is stopped by clot and a new fibrin layer is formed around the rupture point. It is proposed that the cerebrospinal fluid has a special accelerating action in clot formation. This fibrin layer is weak, and repeat rupture occurs within 3 weeks after the initial hemorrhage. However, after 3 weeks, rebleeding is rare due to the reinforcement of this layer, and capillaries appear in this new wall. Hemorrhages from these capillaries occur within and outside the new wall caused by the constant impingement of blood flow. In severe cases, the aneurysm ruptures again, but when the hemorrhages are slight, the aneurysm grows as the wall is thickened by repeated hemorrhages and their absorption. This may explain the growth mechanism of the aneurysm.

Role of estrogen deficiency in the formation and progression of cerebral aneurysms. Part I: experimental study of the effect of oophorectomy in rats

2005 ◽  
Vol 103 (6) ◽  
pp. 1046-1051 ◽  
Author(s):  
Mohammad A. Jamous ◽  
Shinji Nagahiro ◽  
Keiko T. Kitazato ◽  
Junichiro Satomi ◽  
Koichi Satoh
Keyword(s):  
Cerebral Aneurysm ◽  
Cerebral Aneurysms ◽  
Bilateral Oophorectomy ◽  
Gelatinase Activity ◽  
Content Type ◽  
Group Iii ◽  
Group I ◽  
Group Ii ◽  
Fine Print

Object. Estrogen has been shown to play a central role in vascular biology. Although it may exert beneficial vascular effects, its role in the pathogenesis of cerebral aneurysms remains to be determined. To elucidate the role of hormones further, the authors examined the effects of bilateral oophorectomy on the formation and progression of cerebral aneurysms in rats. Methods. Forty-five female, 7-week-old Sprague—Dawley rats were divided into three equal groups. Group I consisted of intact rats (controls). To induce cerebral aneurysms, the animals in Groups II and III were subjected to ligation of the right common carotid and bilateral posterior renal arteries. One month later, the rats in Group II underwent bilateral oophorectomy. Three months after the experiment began all animals were killed and cerebral vascular corrosion casts were prepared and screened for cerebral aneurysms by using a scanning electron microscope. Plasma was used to determine the level of estradiol and the gelatinase activity. Hypertension developed in all rats except those in the control group. The estradiol level was significantly lower in Group II than in the other groups (p < 0.01). The incidence of cerebral aneurysm formation in Group II (60%) was three times higher than that in Group III (20%), and the mean size of aneurysms in Group II (76 ± 27 µm, mean ± standard deviation) was larger than that in Group III (28 ± 4.6 µm) (p < 0.05). No aneurysm developed in control animals (Group I), and there was no significant difference in plasma gelatinase activity among the three groups. Conclusions. The cerebral aneurysm model was highly reproducible in rats. Bilateral oophorectomy increased the susceptibility of rats to aneurysm formation, indicating that hormones play a role in the pathogenesis of cerebral aneurysms.

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