scholarly journals Morphologic Variations of end Trunks of M1 Segment of Middle Cerebral Artery

2019 ◽  
Vol 4 (12) ◽  

Introduction: The middle cerebral artery is divided into four segments: proximal M1, insular M2, opercular M3 and cortical M4. M1 extends from the bifurcation point of ACI at ACA and ACM to the insula threshold, laterally from chiasma opticum, laterally from tractus opticus and caudally from trigonum olfactorium, directed laterally, dorsally and rostrally. Early division of the M1 segment into the final trunk is possible at any of the first points of the limb insulae. Material and methods: The study of the micromorphological and morphometric characteristics of the M1 segment was performed in 25 brain (50 ACM preparations) obtained from autopsy of both sexes of different ages without pathological changes. For the removal of the brain from the skull we used the usual technique of obduction. Results: This segment was arch-shaped, in 32 (64%) arteries, rarely S-shaped, in 12 (24%) arteries, much less straight alignment, in 6 (12%) arteries. The average length of the M1 segment of the S shape was 20.6 ± 3.31mm, with a 19.8 mm 4.41mm arch shape, while the straight shape was 16.9 ± 3.62mm. The average S-shaped diameter was 2.7 ± 0.51 mm, arched 2.6 ± 0.47 mm, straight form 2.6 ± 0.36 mm. Variations of M1 branching were: common in 38 cases, early branching in 12 cases, joint trunk with cortical branch in 9 cases, lateral cortical branch in 21 cases, final bifurcation in 24 cases, final trifurcation in 13 cases, duplication in 1 case and M1 accessory in just 1 case. Conclusion: True bifurcation refers to the division of the M1 segment into two final trunks. In cases where the strong joint cortical branch trunk divides from segment M1, while dividing into two terminal trunk immediately after ACM knee formation, it is described as false branching of M1 segment into three terminal branches.

2007 ◽  
Vol 412 (2) ◽  
pp. 114-117 ◽  
Author(s):  
John C. Ashton ◽  
Rosanna M.A. Rahman ◽  
Shiva M. Nair ◽  
Brad A. Sutherland ◽  
Michelle Glass ◽  
...  

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Alexander Akhmedov ◽  
Remo D Spescha ◽  
Francesco Paneni ◽  
Giovani G Camici ◽  
Thomas F Luescher

Background— Stroke is one of the most common causes of death and long term disability worldwide primarily affecting the elderly population. Lectin-like oxidized LDL receptor 1 (LOX-1) is the receptor for oxidized LDL identified in endothelial cells. Binding of OxLDL to LOX-1 induces several cellular events in endothelial cells, such as activation of transcription factor NF-kB, upregulation of MCP-1, and reduction in intracellular NO. Accumulating evidence suggests that LOX-1 is involved in endothelial dysfunction, inflammation, atherogenesis, myocardial infarction, and intimal thickening after balloon catheter injury. Interestingly, a recent study demonstrated that acetylsalicylic acid (aspirin), which could prevent ischemic stroke, inhibited Ox-LDL-mediated LOX-1 expression in human coronary endothelial cells. The expression of LOX-1 was increased at a transient ischemic core site in the rat middle cerebral artery occlusion model. These data suggest that LOX-1 expression induces atherosclerosis in the brain and is the precipitating cause of ischemic stroke. Therefore, the goal of the present study was to investigate the role of endothelial LOX-1 in stroke using experimental mouse model. Methods and Results— 12-week-old male LOX-1TG generated recently in our group and wild-type (WT) mice were applied for a transient middle cerebral artery occlusion (MCAO) model to induce ischemia/reperfusion (I/R) brain injury. LOX-1TG mice developed 24h post-MCAO significantly larger infarcts in the brain compared to WT (81.51±8.84 vs. 46.41±10.13, n=7, p < 0.05) as assessed morphologically using Triphenyltetrazolium chloride (TTC) staining. Moreover, LOX-1TG showed higher neurological deficit in RotaRod (35.57±8.92 vs. 66.14±10.63, n=7, p < 0.05) and Bederson tests (2.22±0.14 vs. 1.25±0.30, n=9-12, p < 0.05) - two experimental physiological tests for neurological function. Conclusions— Thus, our data suggest that LOX-1 plays a critical role in the ischemic stroke when expressed at unphysiological levels. Such LOX-1 -associated phenotype could be due to the endothelial dysfunction. Therefore, LOX-1 may represent novel therapeutic targets for preventing ischemic stroke.


2020 ◽  
Vol 40 (12) ◽  
pp. 2837-2844 ◽  
Author(s):  
Jan Wenzel ◽  
Dimitrios Spyropoulos ◽  
Julian Christopher Assmann ◽  
Mahtab Ahmad Khan ◽  
Ines Stölting ◽  
...  

Objective: THBD (thrombomodulin) is part of the anticoagulant protein C-system that acts at the endothelium and is involved in anti-inflammatory and barrier-stabilizing processes. A recombinant soluble form of THBD was shown to have protective effects in different organs, but how the endogenous THBD is regulated during ischemia, particularly in the brain is not known to date. The aim of this study was to investigate the role of THBD, especially in brain endothelial cells, during ischemic stroke. Approach and Results: To induce ischemic brain damage, we occluded the middle cerebral artery of mice. We found an increased endothelial expression of Thbd in the peri-infarct area, whereas in the core of the ischemic tissue Thbd expression was decreased compared with the contralateral side. We generated a novel Cre/loxP-based mouse line that allows for the inducible deletion of Thbd specifically in brain endothelial cells, which worsened stroke outcome 48 hours after middle cerebral artery occlusion. Unexpectedly, we found no signs of increased coagulation, thrombosis, or inflammation in the brain but decreased vessel diameters and impaired angiogenesis in the peri-infarct area that led to a reduced overall vessel length 1 week after stroke induction. Conclusions: Endogenous THBD acts as a protective factor in the brain during ischemic stroke and enhances vessel diameter and proliferation. These previously unknown properties of THBD could offer new opportunities to affect vessel function after ischemia and thereby improve stroke outcome.


2009 ◽  
Vol 3 (4) ◽  
pp. 296-301 ◽  
Author(s):  
Ljiljana Vasović ◽  
Sladjana Ugrenović ◽  
Ivan Jovanović

Object The authors describe some of the features of the medial striate branch or recurrent artery of Heubner (RAH). This structure has indisputable functional, neurological, and neurosurgical significance, and originates from the A1 and/or A2 segments of the anterior cerebral artery. Methods Microdissection of 94 human fetal specimens was performed. The RAH was observed in 97.3% (single in 71.6%, double in 25.1%, and triple in 3.3%) of the cases. Its origin was from A2 in 42.3% of specimens, from the A1–A2 junction in 25.7%, and from A1 in 20%. Results Five types and 14 subtypes of the RAH were identified, determined based on vessel origin and number. In its course, the RAH gave 1–12 branches, and the terminal part most frequently penetrated into the brain through the anterior perforated substance at the level of the sphenoid segment of the middle cerebral artery. The specimens with a single RAH fenestration, abnormal double RAH anastomosis, and unusual RAH origin and relationship to the surrounding vessels represented new data. Conclusions The authors' observations of common anatomical variations in the number and origin of the RAH, as well as its abnormalities, may assist neuroradiologists in the interpretation of diagnostic test results and neurosurgeons in performing procedures in the anterior cerebral circulation.


Molecules ◽  
2018 ◽  
Vol 23 (7) ◽  
pp. 1747 ◽  
Author(s):  
Nan Li ◽  
Lingling Feng ◽  
Yujun Tan ◽  
Yan Xiang ◽  
Ruoqi Zhang ◽  
...  

The dry root of Scutellaria baicalensis, has traditionally been applied in the treatment of cerebral ischemia in Chinese clinics. Baicalin (BA) is considered the key ingredient in it for the brain protection effects. The bioavailability of BA is very low because of its poor lipid and water solubility, which limits the therapeutic effects and clinical application. The aim of the present study was to develop a novel BA-loaded liposome (BA-LP) formulation to improve the drug lipophilicity and further to enhance the drug-concentration in the brain tissues. This study is also designed to investigate the pharmacokinetics of BA in the pathological conditions of stroke and evaluate the pharmacokinetic differences of BA caused by stroke after intravenous administration with BA and BA-LP. In this study, the novel BA-LP prepared in early stage were characterized by morphology, size, zeta potential, encapsulation rate and the in vitro release. The pharmacokinetics and biodistribution of BA and BA-LP were investigated by intravenous administration in rats with middle cerebral artery occlusion (MCAO) model and normal group respectively. BA-LP had a mean particle size of 160–190 nm, zeta potential of −5.7 mV, and encapsulation efficiency of 42 ± 1%. The BA-LP showed a sustained-release behavior, the in vitro drug-release kinetic model of BA-LP fit well with the biphasic dynamic model equation: Q = 1 − (60.12e0.56t − 59.08e0.0014t). Pharmacokinetic behavior in MCAO rats is not consistent with that of normal rats. The middle cerebral artery occlusion rats got higher Cmax and AUC0–t, which were about 1.5–2 times to normal rats both in BA and liposome groups. In addition, it got especially higher distribution in brain, while BA were not detected in brain tissues on normal rats. The Cmax and AUC0–t values were significantly greater with liposome than BA on both normal and MCAO rats. The tissue distribution behavior was significantly altered in the case of liposome administrated in comparison with BA, which the concentrations in the heart, liver, spleen, lungs and brain were all increased after administrated liposome, but decreased in kidneys. The TI values showed that the target of liposome was improved especially to heart, spleen and brain, and the brain’s target was higher in striatum and cerebellum. In conclusion, BA-LP might be a potential drug delivery system to improve the therapeutic efficacy of BA. In addition, these results also suggest that the pathological damages of ischemia-reperfusion have a significant impact on the pharmacokinetic traits of BA.


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