scholarly journals Pathomorphological manifestations of vascular remodeling in the perifocal areas of ischemic cerebral infarction

2021 ◽  
Vol 25 (2(98)) ◽  
pp. 22-28
Author(s):  
O. Voloshanska
Keyword(s):  
Blood Flow ◽  
Cerebral Infarction ◽  
Vascular Remodeling ◽  
Blood Circulation ◽  
Capillary Network ◽  
Cerebral Stroke ◽  
Collateral Blood Flow ◽  
Pial Vessels ◽  
Morphological Studies ◽  
The Brain

Abstract. Acute disorders of cerebral circulation remain one of the leading causes of death of patients throughout the world. Tissue recovery after a stroke is directly related to active revascularization, which is intensified in the peri-infarction area. Newly formed vessels contribute to the restoration of cellular metabolism in surviving neurons. The processes of vascular remodeling after stroke have been at the center of many clinical and morphological studies in recent years. The aim of the study. To study the processes of vascular remodeling and neoplasm of vessels in the perifocal areas of ischemic cerebral infarctions. Material and methods. The study researched the brain of 29 deceased patients with hemispheric infarctions with different periods of the disease: up to 3 days (n = 5), 6 days (n = 5), 9-12 (n = 10), 30 (n = 5), 45 days (n = 4). The object of the study was perifocal areas of cerebral infarction, as well as areas outside ischemic lesions. The studies were carried out using histological, morphometric and statistical techniques. Results. Studies have shown that in the perifocal areas of cerebral infarction within 3 days from the onset of the disease, the morpho-functional state of the microvasculature was characterized by circulatory and hemocoagulation disorders. Along with destructive changes in blood vessels, processes are directed to improve blood circulation in ischemic areas of the brain. Collateral blood flow increases, dilation of pial vessels is noted with a decrease in the Kernogan index. On the 6th day, the processes of angiogenesis and vasculogenesis are activated, which intensify in the subsequent stages of the disease. In the long term, the efficiency of collateral blood flow in the pial vessels decreases, reduction in the capillary network, and the lumen of large arteries is recalibrated. Conclusions. In the early stages of cerebral stroke (up to 3 days), increased blood circulation in the ischemic areas of the brain occurs due to increased collateral blood flow. From the 6th day, the processes of angiogenesis in the form of capillary budding and the processes of vasculogenesis intensify. In large arterioles, recalibration processes take place. After 30-45 days in the perifocal areas of cerebral infarction, a significant reduction of the capillary network is recorded, which is regarded as a reaction to a decrease in blood supply to the areas of organized infarction.

scholarly journals Contractile pericytes determine the direction of blood flow at capillary junctions

2020 ◽  
Vol 117 (43) ◽  
pp. 27022-27033
Author(s):  
Albert L. Gonzales ◽  
Nicholas R. Klug ◽  
Arash Moshkforoush ◽  
Jane C. Lee ◽  
Frank K. Lee ◽  
...  
Keyword(s):  
Blood Flow ◽  
Circulatory System ◽  
The Body ◽  
Capillary Network ◽  
Transitional Region ◽  
Capillary Networks ◽  
Efficiency And Effectiveness ◽  
The Central Nervous System ◽  
Essential Function ◽  
The Brain

The essential function of the circulatory system is to continuously and efficiently supply the O2 and nutrients necessary to meet the metabolic demands of every cell in the body, a function in which vast capillary networks play a key role. Capillary networks serve an additional important function in the central nervous system: acting as a sensory network, they detect neuronal activity in the form of elevated extracellular K+ and initiate a retrograde, propagating, hyperpolarizing signal that dilates upstream arterioles to rapidly increase local blood flow. Yet, little is known about how blood entering this network is distributed on a branch-to-branch basis to reach specific neurons in need. Here, we demonstrate that capillary-enwrapping projections of junctional, contractile pericytes within a postarteriole transitional region differentially constrict to structurally and dynamically determine the morphology of capillary junctions and thereby regulate branch-specific blood flow. We further found that these contractile pericytes are capable of receiving propagating K+-induced hyperpolarizing signals propagating through the capillary network and dynamically channeling red blood cells toward the initiating signal. By controlling blood flow at junctions, contractile pericytes within a functionally distinct postarteriole transitional region maintain the efficiency and effectiveness of the capillary network, enabling optimal perfusion of the brain.

scholarly journals Effect of combined VEGF165/SDF-1 gene therapy on vascular remodeling and blood perfusion in cerebral ischemia

2017 ◽  
Vol 127 (3) ◽  
pp. 670-678 ◽  
Author(s):  
Guo-jie Hu ◽  
Yu-gong Feng ◽  
Wen-peng Lu ◽  
Huan-ting Li ◽  
Hong-wei Xie ◽  
...  
Keyword(s):  
Gene Therapy ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Infarction ◽  
Rat Model ◽  
Vascular Remodeling ◽  
Cerebral Blood Volume ◽  
Neural Function ◽  
Triphenyltetrazolium Chloride ◽  
Immunofluorescence Labeling

OBJECTIVETherapeutic neovascularization is a promising strategy for treating patients after an ischemic stroke; however, single-factor therapy has limitations. Stromal cell-derived factor 1 (SDF-1) and vascular endothelial growth factor (VEGF) proteins synergistically promote angiogenesis. In this study, the authors assessed the effect of combined gene therapy with VEGF165 and SDF-1 in a rat model of cerebral infarction.METHODSAn adenoviral vector expressing VEGF165 and SDF-1 connected via an internal ribosome entry site was constructed (Ad-VEGF165-SDF-1). A rat model of middle cerebral artery occlusion (MCAO) was established; either Ad-VEGF165-SDF-1 or control adenovirus Ad-LacZ was stereotactically microinjected into the lateral ventricle of 80 rats 24 hours after MCAO. Coexpression and distribution of VEGF165 and SDF-1 were examined by reverse-transcription polymerase chain reaction, Western blotting, and immunofluorescence. The neurological severity score of each rat was measured on Days 3, 7, 14, 21, and 28 after MCAO. Angiogenesis and vascular remodeling were evaluated via bromodeoxyuridine and CD34 immunofluorescence labeling. Relative cerebral infarction volumes were determined by T2-weighted MRI and triphenyltetrazolium chloride staining. Cerebral blood flow, relative cerebral blood volume, and relative mean transmit time were assessed using perfusion-weighted MRI.RESULTSThe Ad-VEGF165-SDF-1 vector mediated coexpression of VEGF165 and SDF-1 in multiple sites around the ischemic core, including the cortex, corpus striatum, and hippocampal granular layer. Coexpression of VEGF165 and SDF-1 improved neural function, reduced cerebral infarction volume, increased microvascular density and promoted angiogenesis in the ischemic penumbra, and improved cerebral blood flow and perfusion.CONCLUSIONSCombined VEGF165 and SDF-1 gene therapy represents a potential strategy for improving vascular remodeling and recovery of neural function after cerebral infarction.

scholarly journals Collateral Supply in Preclinical Cerebral Stroke Models

2021 ◽  
Author(s):  
Philippe Bonnin ◽  
Nathalie Kubis ◽  
Christiane Charriaut-Marlangue
Keyword(s):  
Blood Flow ◽  
Blood Supply ◽  
Time Course ◽  
Imaging Techniques ◽  
Artery Occlusion ◽  
Added Value ◽  
Cerebral Stroke ◽  
Collateral Blood Flow ◽  
Pial Arteries ◽  
Pharmacological Agents

AbstractEnhancing the collateral blood supply during the acute phase of cerebral ischemia may limit both the extension of the core infarct, by rescuing the penumbra area, and the degree of disability. Many imaging techniques have been applied to rodents in preclinical studies, to evaluate the magnitude of collateral blood flow and the time course of responses during the early phase of ischemic stroke. The collateral supply follows several different routes at the base of the brain (the circle of Willis) and its surface (leptomeningeal or pial arteries), corresponding to the proximal and distal collateral pathways, respectively. In this review, we describe and illustrate the cerebral collateral systems and their modifications following pre-Willis or post-Willis occlusion in rodents. We also review the potential pharmaceutical agents for stimulating the collateral blood supply tested to date. The time taken to establish a collateral blood flow supply through the leptomeningeal anastomoses differs between young and adult animals and between different species and genetic backgrounds. Caution is required when transposing preclinical findings to humans, and clinical trials must be performed to check the added value of pharmacological agents for stimulating the collateral blood supply at appropriate time points. However, collateral recruitment appears to be a rapid, beneficial, endogenous mechanism that can be stimulated shortly after artery occlusion. It should be considered a treatment target for use in addition to recanalization strategies.

VEGF121- and bFGF-induced increase in collateral blood flow requires normal nitric oxide production

2001 ◽  
Vol 280 (3) ◽  
pp. H1097-H1104 ◽  
Author(s):  
H. T. Yang ◽  
Z. Yan ◽  
Judith A. Abraham ◽  
Ronald L. Terjung
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Growth Factors ◽  
Growth Factor ◽  
Vascular Remodeling ◽  
No Production ◽  
Collateral Blood Flow ◽  
Angiogenic Growth Factors ◽  
Blood Flows ◽  
Calf Muscles

The angiogenic proteins basic fibroblast growth factor (bFGF; FGF-2) and vascular endothelial growth factor 121 (VEGF121) are each able to enhance the collateral-dependent blood flow after bilateral femoral artery ligation in rats. To study the effect of nitric oxide (NO) synthase (NOS) inhibition on bFGF- or VEGF121-induced blood flow expansion, the femoral arteries of male Sprague-Dawley rats were ligated bilaterally, and the animals were given tap water [non- NG-nitro-l-arginine methyl ester (l-NAME) group; n = 36] or water that contained l-NAME (l-NAME group; 2 mg/ml, n = 36). Animals from each group were further divided into three subgroups: vehicle ( n = 12), bFGF (5 μg · kg−1· day−1, n = 12), or VEGF121(10 μg · kg−1· day−1, n = 12). Growth factors were delivered via intra-arterial infusion with osmotic pumps over days 1–14. On day 16, after a 2-day delay to permit clearance of bFGF and VEGF from the circulation, maximal collateral blood flow was determined by85Sr- and141Ce-labeled microspheres during treadmill running.l-NAME (∼137 mg · kg−1· day−1) for 18 days increased systemic blood pressure (∼26%, P < 0.001). In the absence of l-NAME, collateral-dependent blood flows to the calf muscles were greater in the VEGF121- and bFGF-treated subgroups (85 ± 4.5 and 80 ± 2.9 ml · min−1· 100 g−1, respectively) than in the vehicle subgroup (49 ± 3.0 ml · min−1· 100 g−1, P < 0.001). In the presence of NOS inhibition byl-NAME, blood flows to the calf muscles were essentially equivalent among the three subgroups (54 ± 3.0, 56 ± 5.1, and 47 ± 2.0 ml · min−1· 100 g−1in the bFGF-, VEGF121-, and vehicle-treated subgroups, respectively) and were not different from the blood flow in the non-l-NAME vehicle subgroup. Our results therefore indicate that normal NO production is essential for the enhanced vascular remodeling induced by exogenous bFGF or VEGF121in this rat model of experimental peripheral arterial insufficiency. These results imply that a blunted endothelial NO production could temper vascular remodeling in response to these angiogenic growth factors.

scholarly journals Acute Onset Asymmetric Sensorimotor Paraparesis: Not Always Spinal!

2020 ◽  
Vol 3 (1) ◽  
pp. 40-42
Author(s):  
Dhananjay Gupta ◽  
Pradeep R ◽  
Anish Mehta ◽  
Mahendra Javali ◽  
Purshottam T. Acharya ◽  
...  
Keyword(s):  
Magnetic Resonance Imaging ◽  
Magnetic Resonance ◽  
Cerebral Infarction ◽  
Symptomatic Improvement ◽  
Acute Onset ◽  
Lower Limbs ◽  
Sensory Loss ◽  
Cerebral Stroke ◽  
Resonance Imaging ◽  
The Brain

Objective: To report an atypical case of acute onset sensorimotor paraparesis secondary to bilateral cerebral stroke. Background: Acute onset paraparesis or paraplegia is usually secondary to a spinal cord disease. Central or cerebral causes of paraparesis are rare and include parasagittal and bilateral precentral lesions. Design/Methods: Case report and literature review. Results: A 65-year-old man presented with acute onset weakness of both lower limbs, associated with pins and needle sensation. On examination, he was found to have paraparesis (grade 2/5, both legs) and an asymmetric sensory loss in both legs and thighs. Spinal magnetic resonance imaging ruled out any compressive or noncompressive etiology. Magnetic resonance imaging of the brain showed an acute infarction in the bilateral cerebral hemisphere in both the pre- and postcentral gyrus. An angiogram of the brain revealed an aplastic right ACA-A1 with left ACA-A1 feeding bilateral A2. There was distal left ACA-A1 stenosis seen, the probable cause of bilateral stroke in this patient. The patient was treated conservatively and showed symptomatic improvement during the course of stay at the hospital. Conclusion: This case of acute paraparesis secondary to bilateral cerebral infarction demonstrates the need to always look for a cerebral cause. In patients with cerebral infarction, who present early to a hospital, it may provide a window for thrombolytic or endovascular therapy.

scholarly journals Anti-Inflammatory Dipeptide, a Metabolite from Ambioba Secretion, Protects Cerebral Ischemia Injury by Blocking Apoptosis Via p-JNK/Bax Pathway

2021 ◽  
Vol 12 ◽  
Author(s):  
Qian Zhang ◽  
Jinwei Dai ◽  
Zhibing Song ◽  
Yuchen Guo ◽  
Shanshan Deng ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Blood Flow ◽  
Superoxide Dismutase ◽  
Cerebral Ischemia ◽  
Cerebral Infarction ◽  
Neuroprotective Effect ◽  
Survival Rates ◽  
Oxygen Species ◽  
The Brain ◽  
Monocyte Locomotion Inhibitory Factor

MQ (l-methionyl-l-glutamic acid), anti-inflammatory dipeptide, is one of the metabolites of monocyte locomotion inhibitory factor, a thermostable pentapeptide secreted by Entamoeba histolytica. Monocyte locomotion inhibitory factor injection has been approved as an investigational drug for the potential neural protection in acute ischemic stroke. This study further investigated the neuroprotective effect of MQ in ischemic brain damage. Ischemia-reperfusion injury of the brain was induced in the rat model by middle cerebral artery occlusion. 2,3,5-triphenyltetrazolium chloride staining assay was used to measure cerebral infarction areas in rats. Laser Doppler measurement instrument was used to detect blood flow changes in the rat model. Nissl staining and NeuN staining were utilized to observe the numbers and structures of neuron cells, and the pathological changes in the brain tissues were examined by hematoxylin–eosin staining. Terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick end labeling (TUNEL) staining was used to assess cell apoptosis. The changes in oxidative stress indexes, superoxide dismutase and malondialdehyde (MDA), were measured in serum. Methyl thiazolyl tetrazolium was used to measure the survival rates of PC12 cells. Flow cytometry assessed the apoptosis rates and the levels of reactive oxygen species. Real-time PCR was used to evaluate the mRNA expression levels, and Western blotting was used to analyze the changes in protein levels of p-JNK, Bax, cleaved Caspase3. We revealed that MQ improved neurobehavior, decreased cerebral infarction areas, altered blood flow volume, and the morphology of the cortex and hippocampus. On the other hand, it decreased the apoptosis of cortical neurons and the levels of MDA, and increased the levels of superoxide dismutase. In vitro studies demonstrated that MQ enhanced the cell survival rates and decreased the levels of reactive oxygen species. Compared to the oxygen-glucose deprivation/reperfusion group, the protein and mRNA expressions of p-JNK, Bax, cleaved Caspase3 was decreased significantly. These findings suggested that MQ exerts a neuroprotective effect in cerebral ischemia by blocking apoptosis via the p-JNK/Bax pathway.

Microvascular features that suggest effectors of blood-flow regulation in the brain: Evidence by SEM of corrosion casts of intracerebral vessels

1990 ◽  
Vol 48 (3) ◽  
pp. 274-275
Author(s):  
Enrico D.F. Motti ◽  
Hans-Georg Imhof ◽  
Gazi M. Yasargil
Keyword(s):  
Blood Flow ◽  
Perfusion Pressure ◽  
Corrosion Casts ◽  
Cerebral Microcirculation ◽  
Pial Arteries ◽  
Random Occurrence ◽  
Brain Arteries ◽  
Homogeneous Network ◽  
The Brain

Physiologists have devoted most attention in the cerebrovascular tree to the arterial side of the circulation which has been subdivided in three levels: 1) major brain arteries which keep microcirculation constant despite changes in perfusion pressure; 2) pial arteries supposed to be effectors regulating microcirculation; 3) intracerebral arteries supposed to be deprived of active cerebral blood flow regulating devices.The morphological search for microvascular effectors in the cerebrovascular bed has been elusive. The opaque substance of the brain confines in vivo investigation to the superficial pial arteries. Most morphologists had to limit their observation to the random occurrence of a favorable site in the practically two-dimensional thickness of diaphanized histological sections. It is then not surprising most investigators of the cerebral microcirculation refer to an homogeneous network of microvessels interposed between arterioles and venules.We have taken advantage of the excellent depth of focus afforded by the scanning electron microscope (SEM) to investigate corrosion casts obtained injecting a range of experimental animals with a modified Batson's acrylic mixture.

Fit Vs Faint: Assessing Work Causation in “Idiopathic Fall” Cases

2014 ◽  
Vol 19 (5) ◽  
pp. 3-12
Author(s):  
Lorne Direnfeld ◽  
David B. Torrey ◽  
Jim Black ◽  
LuAnn Haley ◽  
Christopher R. Brigham
Keyword(s):  
Blood Flow ◽  
Electrical Activity ◽  
Loss Of Consciousness ◽  
Brain Electrical Activity ◽  
Medical Terminology ◽  
Scientific Analysis ◽  
Medical Causation ◽  
The Individual ◽  
The Brain ◽  
Current Science

Abstract When an individual falls due to a nonwork-related episode of dizziness, hits their head and sustains injury, do workers’ compensation laws consider such injuries to be compensable? Bearing in mind that each state makes its own laws, the answer depends on what caused the loss of consciousness, and the second asks specifically what happened in the fall that caused the injury? The first question speaks to medical causation, which applies scientific analysis to determine the cause of the problem. The second question addresses legal causation: Under what factual circumstances are injuries of this type potentially covered under the law? Much nuance attends this analysis. The authors discuss idiopathic falls, which in this context means “unique to the individual” as opposed to “of unknown cause,” which is the familiar medical terminology. The article presents three detailed case studies that describe falls that had their genesis in episodes of loss of consciousness, followed by analyses by lawyer or judge authors who address the issue of compensability, including three scenarios from Arizona, California, and Pennsylvania. A medical (scientific) analysis must be thorough and must determine the facts regarding the fall and what occurred: Was the fall due to a fit (eg, a seizure with loss of consciousness attributable to anormal brain electrical activity) or a faint (eg, loss of consciousness attributable to a decrease in blood flow to the brain? The evaluator should be able to fully explain the basis for the conclusions, including references to current science.

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