Microangiopathy (MAP) in the distal arterial bed develops in the structures high in pericytes that have myofibrils and, by interacting with the endothelium, form the first peristaltic pumps; they push lymph, hemolymph and blood from the arterial bed to the venous one. The role of glucose, hyperglycemia, a glycation reaction and its end products in microvascular interstitial tissue damage in the arterial bed is shown only in the neuron axon terminals that surround the pool of the intercellular medium while the other axonal parts are present in the cerebrospinal fluid pool where hyperglycemia is absent. When glucose metabolism is activated through the poliolovic pathway, the endothelial cytosole accumulates organic osmolytes, such as sorbitol alcohol that, by causing hyperhydration, increases the height of endothelial cells. The decreased lumen of arterioles and capillaries enhances peripheral resistance to blood flow to give rise hypoperfusion and chronic hypoxia. Moreover, by bypassing the exchange capillaries and worsening cellular hypoperfusion and hypoxia in the paracrine communities, the arteriolo-venular shunt that releases blood into the venous bed functions, by getting around the exchange capillaries. Glucose metabolism activation through the hexosamine pathway generates glycotoxins, such as glyoxal and methylglyoxal. As bifunctional reagents, they interact with proteins simultaneously, by using both ends, form cross-links between the collagen fibers in the vascular interstitial matrix and irreversibly enhance the rigidity of arteriolar and capillary walls. As the rigidity of the walls is increased, the pericytes are unable to move blood along the capillaries, by worsening hypoperfusion and hypoxia. In diabetes, hyperglycemia becomes persistent and glycation increased. The conversion of collagen structured in the vascular wall to glycosylation end products and the impaired biological function of endoecology are a cause of a biological reaction of interstitial tissue inflammation. The obligate part of the biological reaction of inflammation is the oxidation by reactive oxygen species and the generation of malondialdehyde, that is also a bifunctional reagent. Fibroblast proliferation and arteriosclerosis are a result of MAP as a destructive inflammatory process in the arteriolar and capillary walls.
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AJNR Am J Neuroradiol
January 2025
From the Tu Lab for Diagnostic Research, Yale School of Medicine, New Haven, CT, USA (OAZ, AEK, SR) and Department of Radiology and Biomedical Imaging, Yale School of Medicine, New Haven, CT, USA (IDOS, JJ, LHT).
Background And Purpose: Timely reporting of CTA exams impacts management of acute vascular pathology such as large vessel occlusions, arterial dissection, and ruptured aneurysm as well as a variety of acute non-vascular pathologies. In this study, we examine potential modifiable factors impacting the timeliness of CTA reporting performed in stroke code activations.
Materials And Methods: Observational study of stroke code CTA head and neck exams performed at a single health system (3 emergency departments, 1550 inpatient beds) over four years (1/1/2019-12/31/2023).
Indian J Thorac Cardiovasc Surg
February 2025
Sechenov First Moscow State Medical University, Moscow, Russia.
Pulmonary arteriovenous malformation (PAVM) is a congenital vascular pathology, which is caused by the presence of a direct connection between the branches of the artery and the veins of the lungs, and the discharge of unoxygenated blood into the arterial bed. Arteriovenous malformations are characterized by a wide variety of clinical manifestations and, in some cases, may be accompanied with severe circulatory disorders.
View Article and Find Full Text PDFJVS Vasc Insights
May 2024
Yale Cardiovascular Research Center, Section of Cardiovascular Medicine, Department of Internal Medicine, Yale University.
Objective: Atherosclerosis underlies the most common etiologies of mortality worldwide, resulting in nearly 10 million deaths annually. In atherosclerosis, inflammation, metabolic factors, and hemodynamics cause the accumulation of extracellular lipids and the formation of plaques in the tunica intima of specific arteries. Atherosclerotic plaques primarily form in the coronary and carotid arteries, the aorta, and the peripheral arteries of the lower extremities.
View Article and Find Full Text PDFRev Med Liege
January 2025
Service de Pneumologie, CHU Liège, Belgique.
Idiopathic pulmonary arterial hypertension (iPAH) is a rare, rapidly progressive disease associated with high morbidity and mortality. It is characterized by endothelial dysfunction within the pulmonary vascular bed and gradually leads to an increase in the pulmonary vascular resistances. Its non-specific symptomatology delays the diagnosis and brings the most severe forms to right ventricular failure.
View Article and Find Full Text PDFVasc Biol
January 2025
M Daemen, Pathology, Amsterdam UMC Location AMC, Amsterdam, Netherlands.
Background: Although mice are used extensively to study atherosclerosis of different vascular beds, limited data is published on the occurrence of intracranial atherosclerosis. Since intracranial atherosclerosis is a common cause of stroke and is associated with dementia, a relevant animal model is needed to study these diseases.
Methods And Results: We examined the presence of intracranial atherosclerosis in different atherogenic mouse strains and studied differences in vessel wall characteristics in mouse and human tissue in search for possible explanations for the different atherosclerotic susceptibility between extracranial and intracranial vessels.
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