Intimal hyperplasia: The permeation of serum-derived substance into the arterial autovein graft under abnormal blood flow

1988 ◽  
Vol 18 (3) ◽  
pp. 300-307 ◽  
Author(s):  
Masazumi Kuroki ◽  
Kenichiro Okadome ◽  
Kiyoshi Inokuchi ◽  
Keizo Sugimachi
Keyword(s):  
Blood Flow ◽  
Intimal Hyperplasia

scholarly journals The role of oxygen transport in atherosclerosis and vascular disease

2020 ◽  
Vol 17 (165) ◽  
pp. 20190732 ◽  
Author(s):  
John Tarbell ◽  
Marwa Mahmoud ◽  
Andrea Corti ◽  
Luis Cardoso ◽  
Colin Caro
Keyword(s):  
Blood Flow ◽  
Vascular Disease ◽  
Oxygen Transport ◽  
Intimal Hyperplasia ◽  
Hypoxia Inducible Factor ◽  
Vascular Diseases ◽  
Vascular Wall ◽  
Vasa Vasorum ◽  
Mechanical Factors

Atherosclerosis and vascular disease of larger arteries are often associated with hypoxia within the layers of the vascular wall. In this review, we begin with a brief overview of the molecular changes in vascular cells associated with hypoxia and then emphasize the transport mechanisms that bring oxygen to cells within the vascular wall. We focus on fluid mechanical factors that control oxygen transport from lumenal blood flow to the intima and inner media layers of the artery, and solid mechanical factors that influence oxygen transport to the adventitia and outer media via the wall's microvascular system—the vasa vasorum (VV). Many cardiovascular risk factors are associated with VV compression that reduces VV perfusion and oxygenation. Dysfunctional VV neovascularization in response to hypoxia contributes to plaque inflammation and growth. Disturbed blood flow in vascular bifurcations and curvatures leads to reduced oxygen transport from blood to the inner layers of the wall and contributes to the development of atherosclerotic plaques in these regions. Recent studies have shown that hypoxia-inducible factor-1α (HIF-1α), a critical transcription factor associated with hypoxia, is also activated in disturbed flow by a mechanism that is independent of hypoxia. A final section of the review emphasizes hypoxia in vascular stenting that is used to enlarge vessels occluded by plaques. Stenting can compress the VV leading to hypoxia and associated intimal hyperplasia. To enhance oxygen transport during stenting, new stent designs with helical centrelines have been developed to increase blood phase oxygen transport rates and reduce intimal hyperplasia. Further study of the mechanisms controlling hypoxia in the artery wall may contribute to the development of therapeutic strategies for vascular diseases.

scholarly journals Increased Blood Flow Induces Regression of Intimal Hyperplasia

1997 ◽  
Vol 17 (10) ◽  
pp. 2245-2249 ◽  
Author(s):  
Erney J. R. Mattsson ◽  
Ted R. Kohler ◽  
Selina M. Vergel ◽  
Alexander W. Clowes
Keyword(s):  
Blood Flow ◽  
Intimal Hyperplasia ◽  
Increased Blood Flow

A new RXR agonist, HX630, suppresses intimal hyperplasia in a mouse blood flow cessation model

2006 ◽  
Vol 41 (5) ◽  
pp. 885-892 ◽  
Author(s):  
Go Haraguchi ◽  
Jun-ichi Suzuki ◽  
Hisanori Kosuge ◽  
Masahito Ogawa ◽  
Noritaka Koga ◽  
...  
Keyword(s):  
Blood Flow ◽  
Intimal Hyperplasia ◽  
Mouse Blood

Reduced blood flow accelerates intimal hyperplasia in endarterectomized canine arteries

1995 ◽  
Vol 3 ◽  
pp. 25-25
Author(s):  
C CHEN ◽  
S MATTAR ◽  
K COYLE ◽  
A LUMSDEN ◽  
D KU
Keyword(s):  
Blood Flow ◽  
Intimal Hyperplasia

scholarly journals Calcium Phosphate Bions Cause Intimal Hyperplasia in Intact Aortas of Normolipidemic Rats through Endothelial Injury

2019 ◽  
Vol 20 (22) ◽  
pp. 5728 ◽  
Author(s):  
Daria Shishkova ◽  
Elena Velikanova ◽  
Maxim Sinitsky ◽  
Anna Tsepokina ◽  
Olga Gruzdeva ◽  
...  
Keyword(s):  
Blood Flow ◽  
Calcium Phosphate ◽  
Intimal Hyperplasia ◽  
Serum Proteins ◽  
Physiological Saline ◽  
Endothelial Injury ◽  
Reactive Protein ◽  
Calcium Deposits ◽  
Organic Particles ◽  
Injection Regimen

Calcium phosphate bions (CPBs) are formed under blood supersaturation with calcium and phosphate owing to the mineral chaperone fetuin-A and representing mineralo-organic particles consisting of bioapatite and multiple serum proteins. While protecting the arteries from a rapid medial calcification, CPBs cause endothelial injury and aggravate intimal hyperplasia in balloon-injured rat aortas. Here, we asked whether CPBs induce intimal hyperplasia in intact rat arteries in the absence of cardiovascular risk factors. Normolipidemic Wistar rats were subjected to regular (once/thrice per week over 5 weeks) tail vein injections of either spherical (CPB-S) or needle-shaped CPBs (CPB-N), magnesium phosphate bions (MPBs), or physiological saline (n = 5 per group). Neointima was revealed in 3/10 and 4/10 rats which received CPB-S or CPB-N, respectively, regardless of the injection regimen or blood flow pattern in the aortic segments. In contrast, none of the rats treated with MPBs or physiological saline had intimal hyperplasia. The animals also did not display signs of liver or spleen injury as well as extraskeletal calcium deposits. Serum alanine/aspartate transaminases, interleukin-1β, MCP-1/CCL2, C-reactive protein, and ceruloplasmin levels did not differ among the groups. Hence, CPBs may provoke intimal hyperplasia via direct endothelial injury regardless of their shape or type of blood flow.

scholarly journals Participation of kinins in the captopril-induced inhibition of intimal hyperplasia caused by interruption of carotid blood flow in the mouse

2000 ◽  
Vol 130 (5) ◽  
pp. 1076-1082 ◽  
Author(s):  
Costanza Emanueli ◽  
Maria Bonaria Salis ◽  
Carlos Figueroa ◽  
Julie Chao ◽  
Lee Chao ◽  
...  
Keyword(s):  
Blood Flow ◽  
Intimal Hyperplasia ◽  
Carotid Blood Flow
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