scholarly journals Hypothetical Pathway for Formation of Cholesterol Microcrystals Initiating the Atherosclerotic Process

2020 ◽  
Vol 78 (3) ◽  
pp. 241-247
Author(s):  
Witold K. Subczynski ◽  
Marta Pasenkiewicz-Gierula
Keyword(s):  
Oxidative Stress ◽  
Blood Vessel ◽  
Plasma Membranes ◽  
Formation Pathway ◽  
Atherosclerotic Plaque Formation ◽  
Arterial Intima ◽  
Phospholipid Peroxidation ◽  
Vessel Walls ◽  
Atherosclerotic Process ◽  
Major Factors

Abstract Major factors leading to the development of atherosclerosis are a high cholesterol (Chol) level in the blood and oxidative stress. Both promote the formation of Chol microcrystals in blood vessel walls. Deposition of Chol microcrystals in arterial intima causes inflammation, which initiates and accompanies the atherosclerotic process in all its phases. One of the possible sources of Chol in the blood vessel walls is oxidized low-density lipoproteins—this atherosclerotic plaque formation pathway has already been described in the literature. Here, we hypothesize that initiation of the atherosclerotic process may involve Chol domains in the plasma membranes of arterial cells. Increased Chol content and the presence of polyunsaturated phospholipids in these membranes together with oxidative stress (phospholipid peroxidation) may lead to the formation of pure Chol bilayer domains that, with further peroxidation and increased Chol content, may collapse in the form of Chol seed crystals. Independent of their origin, Chol microcrystals activate inflammasomes, thereby stimulate immune responses, and initiate inflammation that may lead to the development of atherosclerosis. This new, hypothetical pathway has not yet been investigated in depth; however, data from the literature and our own results support its feasibility.

scholarly journals The effect of cigarette smoking on endothelial damage and atherosclerosis development – modeled and analyzed using Petri nets

2017 ◽  
Vol 27 (2) ◽  
pp. 211-228 ◽  
Author(s):  
Kaja Chmielewska ◽  
Dorota Formanowicz ◽  
Piotr Formanowicz
Keyword(s):  
Oxidative Stress ◽  
Petri Nets ◽  
Tobacco Smoke ◽  
Endothelial Damage ◽  
Dual Function ◽  
Contributing Factors ◽  
Atherosclerotic Plaque Formation ◽  
Atherosclerosis Development ◽  
The Impact

Abstract Atherosclerosis as one of the crucial causes of cardiovascular diseases (CVD) is the leading reason of death worldwide. One of the contributing factors to this phenomenon is endothelial dysfunction, which is associated with the impact of various agents and their interactions. Tobacco smoke is one of the well known factors here. For better understanding of its significance a model of its impact on atherosclerotic plaque formation has been proposed. The model contains selected aspects of the influence of tobacco smoke, dual function of nitric oxide (NO) (influence of various mechanisms on NO bioavailability), oxidative stress which promotes low density lipoproteins oxidation, macrophages significance and other mechanisms leading to an aggravation of the endothelial disturbances. The model has been built using Petri nets theory and the analysis has been based on t-invariants. This approach allowed to confirm the important role of inflammation and oxidative stress in atherosclerosis development and moreover it has shown the considerable influence of the cigarette smoke.

LEUKOTRIENES INDUCE THE ACUTE RELEASE OF TISSUE-TYPE PLASMINOGEN ACTIVATOR FROM PERFUSED RAT BLOOD VESSEL WALLS

1987 ◽  
Author(s):  
N Tranquille ◽  
J J Emeis
Keyword(s):  
Blood Vessel ◽  
Plasminogen Activator ◽  
Prostaglandin E1 ◽  
Tissue Type ◽  
Tissue Type Plasminogen Activator ◽  
Type Plasminogen Activator ◽  
Acute Increase ◽  
Vessel Walls ◽  
Isolated Rat

In a previous publication (Blood 66, 86, 1985) we suggested, on the basis of inhibitor experiments, that lipoxygenase metabolites might be involved in the release of tissue-type plasminogen activator (t-PA) from vessel walls. To test this suggestion, isolated rat hindlegs were freed of blood with Tyrode-BSA solution, and subsequently perfused with Tyrode-BSA containing various lipoxygenase metabolites. The perfusate was collected at timed intervals and assayed for t-PA activity by a spectrophoto-metric procedure. Of the compounds tested (see Table) 5-HETE did not induce PA release. However, leukotriene (LT) C4 and LTD4 dose-dependently (10-200 nM) induced the release of t-PA, which plateaued at 160 and 200 nM, respectively. Peak levels of t-PA activity were found at one minute, although the amount of t-PA released was less than that induced by PAF-acether. The PA activity released proved to be t-PA by functional and immunological criteria. Release of t-PA induced by LTC4 and LTD 4 was inhibited by the LT receptor antagonist FPL-55712 (10 μM).Prostaglandin E1 and E2, prostacyclin and ZK 36374 did not induce acute t-PA release at 0.1-2.8 μM concentrations in our model. LTC4 and LTD4 also induced an acute increase of t-PA activity in vivo in rats at a dosage of 2 μg/kg i.v.The data show that LTC4 and LTD4 can directly induce the acute release of t-PA, possibly by interacting with an endothelial LT receptor.

scholarly journals Prolyl 4‐hydroxylase subunit alpha 1 (P4HA1) is a biomarker of poor prognosis in primary melanomas, and its depletion inhibits melanoma cell invasion and disrupts tumor blood vessel walls

2020 ◽  
Vol 14 (4) ◽  
pp. 742-762 ◽  
Author(s):  
Johanna Eriksson ◽  
Vadim Le Joncour ◽  
Tiina Jahkola ◽  
Susanna Juteau ◽  
Pirjo Laakkonen ◽  
...  
Keyword(s):  
Blood Vessel ◽  
Melanoma Cell ◽  
Cell Invasion ◽  
Poor Prognosis ◽  
Tumor Blood Vessel ◽  
Vessel Walls

Presence of Afferent Nerve Fibers in Meningeal Blood Vessel Walls.

1929 ◽  
Vol 26 (4) ◽  
pp. 288-289
Author(s):  
C. D. Leake ◽  
A. G. Kammer ◽  
J. B. Hitz
Keyword(s):  
Blood Vessel ◽  
Nerve Fibers ◽  
Afferent Nerve ◽  
Afferent Nerve Fibers ◽  
Vessel Walls

Determination of a Pressure Drop in the Arteriovenous Fistula With Fluid Structure Interaction Simulations and In Vitro Methods

2017 ◽  
Author(s):  
Daniel Jodko ◽  
Tomasz Palczynski ◽  
Piotr Reorowicz ◽  
Kacper Miazga ◽  
Damian Obidowski ◽  
...  
Keyword(s):  
Pressure Drop ◽  
Blood Vessel ◽  
Arteriovenous Fistula ◽  
In Vitro Model ◽  
Experimental Methods ◽  
Measurement Methods ◽  
Patient Specific ◽  
Vessel Walls ◽  
Vitro Model

A pressure drop and its oscillations occurring in the arteriovenous fistula due to sudden changes in the velocity vector direction or the transitional or turbulent flow, related to its complicated geometry, can exert a significant impact on the blood vessel wall behaviour. On the other hand, the pressure drop cannot be precisely measured in vivo with non-invasive measurement methods. The aim of this study is to assess the pressure drop with numerical and experimental methods in the patient-specific fistula model taking into account a pulsating nature of the flow and the elasticity of blood vessel walls. An additional target is to find a correlation between these two methods. FSI and in vitro simulations of the blood flow were performed for a patient-specific model of the fistula. Basic geometrical data of the correctly functioning mature fistula were obtained with angio-computed tomography. Those data were applied to develop a spatial CAD model of the fistula, which allowed for creating a virtual model for computer simulations and an analogous in vitro model made with rapid prototyping techniques. The material used to build the in vitro model is characterised by mechanical properties similar to the arterial tissue. A non-stationary computer simulation was carried out with an ANSYS software package, keeping as many flow similarities to the experiments carried out on the test stand as possible, and where the blood mimicking fluid was a water solution of glycerine. During the experiments, the static pressure was measured downstream and upstream of the anastomosis with precise pressure transducers. The pressure drop was determined with the numerical and experimental methods, which take into account the elasticity of blood vessels. This is a novel approach, since most of similar studies were conducted on the assumption of rigid blood vessel walls. The obtained results show that the pressure drop within the fistula is not so high as reported in the literature, which is correlated with the precision of measurement methods and the fact that a large portion of the fluid energy is accumulated by the elastic walls.

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