Cerebral Vascular System

2015 ◽  
pp. 985-1011 ◽  
Author(s):  
Oscar U. Scremin
1962 ◽  
Vol 7 (6) ◽  
pp. 545-559 ◽  
Author(s):  
B. M. STEIN ◽  
W. F. McCORMICK ◽  
J. N. RODRIGUEZ ◽  
J. M. TAVERAS

1934 ◽  
Vol 30 (2) ◽  
pp. 207-207
Author(s):  
Е. Kretschmer

Kretschmer introduces a new concept of "cerebral vascular weakness" by analogy, or, as a. himself says, in the same sense in which they speak in relation to another part of the vascular system, "cardiac weakness".


2003 ◽  
Vol 23 (3) ◽  
pp. 320-330 ◽  
Author(s):  
Zhao Zhong Chong ◽  
Jing-Qiong Kang ◽  
Kenneth Maiese

Erythropoietin (EPO) plays a prominent role in the regulation of the hematopoietic system, but the potential function of this trophic factor as a cytoprotectant in the cerebral vascular system is not known. The authors examined the ability of EPO to modulate a series of death-related cellular pathways during free radical–induced injury in cerebral microvascular endothelial cells (ECs). Endothelial cell injury was evaluated by trypan blue, DNA fragmentation, membrane phosphatidylserine exposure, apoptotic protease–activating factor-1 (Apaf-1), and Bcl-xL expression, mitochondrial membrane potential, cytochrome c release, and cysteine protease activity. They show that constitutive EPO is present in ECs but is insufficient to prevent cellular injury. Signaling through the EPO receptor, however, remains biologically responsive to exogenous EPO administration to offer significant protection against nitric oxide–induced injury. Exogenous EPO maintains both genomic DNA integrity and cellular membrane asymmetry through parallel pathways that prevent the induction of Apaf-1 and preserve mitochondrial membrane potential in conjunction with enhanced Bcl-xL expression. Consistent with the modulation of Apaf-1 and the release of cytochrome c, EPO also inhibits the activation of caspase-9 and caspase-3–like activities. Identification of novel cytoprotective pathways used by EPO may serve as therapeutic targets for cerebral vascular disease.


2021 ◽  
Author(s):  
Leonardo Daniel Reis Santos ◽  
Omar Pereira de Almeida Neto ◽  
Michelle Franco Macedo de Lima ◽  
Nathália Varano

Context: Cardiac tumors are rare and myxomas are the most prevalent between them. Although histologically benign, they may cause severe effects given their intracardiac location. Unspecific symptoms compromise the diagnosis, leading to complications such as changes in the cerebral vascular dynamics. Case report following the CARE guidelines. Case report: A 62-year-old woman was admitted to a high complexity hospital in Minas Gerais, with history of unstable angina, aphasia, right hemiparesis, dysarthria, claiming precordialgia with strong intensity. Complained hyporexia and weight loss during the last month. Medical history of 7 transient ischemic attacks (TIA) in the last two years. Physical examination with no abnormalities. Chest x-ray and transesophageal echocardiogram showed bilateral neovascularization and 4.9 x 2.9 cm dimension mass in the left atrium. Coronary angiography revealed proximal calcification and atherosclerotic plaque occluding 40% of the flux in the middle third of the anterior descending artery, pointing to the coexistence of coronary disease and left atrial myxoma. The occurrence of a TIA was determined and the prescription of an anticoagulant to avoid future embolic events. A surgical approach was necessary. Biopsy concluded myxoid and hyaline-rich stroma tumor, evident vascular system, star-shaped cells isolated or forming small groups, confirming myxoma diagnosis. After a ten-day hospitalization, the patient was clinically stable, and was discharged after health education. Conclusion: Cardiac tumors such as myxomas lead to important cerebral vascular consequences, so that the clinical investigation is essential to the differential diagnosis between a stroke and the TIA, to provide adequate treatment and disease prevention.


1967 ◽  
Vol 18 (2) ◽  
pp. 239-252 ◽  
Author(s):  
G.I. Mchedlishvili ◽  
L.G. Ormotsadze ◽  
L.S. Nikolaishvili ◽  
D.G. Baramidze

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