Repair in arterial tissue

1983 ◽  
Vol 399 (3) ◽  
pp. 307-316 ◽  
Author(s):  
J. Chemnitz ◽  
B. Collatz Christensen
Keyword(s):  
Arterial Tissue

scholarly journals THE METABOLISM OF ARTERIAL TISSUE

1949 ◽  
Vol 179 (1) ◽  
pp. 113-118 ◽  
Author(s):  
S. Chernick ◽  
Paul A. Srere ◽  
I.L. Chaikoff
Keyword(s):  
Arterial Tissue

Non-linear imaging and characterization of atherosclerotic arterial tissue using combined SHG and FLIM microscopy

2015 ◽  
Vol 8 (4) ◽  
pp. 347-356 ◽  
Author(s):  
Riccardo Cicchi ◽  
Enrico Baria ◽  
Christian Matthäus ◽  
Marta Lange ◽  
Annika Lattermann ◽  
...  
Keyword(s):  
Arterial Tissue ◽  
Non Linear

Repair in Arterial Tissue

1977 ◽  
Vol 14 (2) ◽  
pp. 116-127
Author(s):  
Bent Collatz Christensen ◽  
Izabella Tkocz
Keyword(s):  
Arterial Tissue

scholarly journals In Silico Prediction of the Mechanobiological Response of Arterial Tissue: Application to Angioplasty and Stenting

2011 ◽  
Vol 133 (8) ◽  
Author(s):  
Colin J. Boyle ◽  
Alexander B. Lennon ◽  
Patrick J. Prendergast
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Time Course ◽  
Neointimal Hyperplasia ◽  
Cell Activity ◽  
Tissue Response ◽  
Cell Phenotype ◽  
Modeling Approach ◽  
Arterial Tissue

One way to restore physiological blood flow to occluded arteries involves the deformation of plaque using an intravascular balloon and preventing elastic recoil using a stent. Angioplasty and stent implantation cause unphysiological loading of the arterial tissue, which may lead to tissue in-growth and reblockage; termed “restenosis.” In this paper, a computational methodology for predicting the time-course of restenosis is presented. Stress-induced damage, computed using a remaining life approach, stimulates inflammation (production of matrix degrading factors and growth stimuli). This, in turn, induces a change in smooth muscle cell phenotype from contractile (as exists in the quiescent tissue) to synthetic (as exists in the growing tissue). In this paper, smooth muscle cell activity (migration, proliferation, and differentiation) is simulated in a lattice using a stochastic approach to model individual cell activity. The inflammation equations are examined under simplified loading cases. The mechanobiological parameters of the model were estimated by calibrating the model response to the results of a balloon angioplasty study in humans. The simulation method was then used to simulate restenosis in a two dimensional model of a stented artery. Cell activity predictions were similar to those observed during neointimal hyperplasia, culminating in the growth of restenosis. Similar to experiment, the amount of neointima produced increased with the degree of expansion of the stent, and this relationship was found to be highly dependant on the prescribed inflammatory response. It was found that the duration of inflammation affected the amount of restenosis produced, and that this effect was most pronounced with large stent expansions. In conclusion, the paper shows that the arterial tissue response to mechanical stimulation can be predicted using a stochastic cell modeling approach, and that the simulation captures features of restenosis development observed with real stents. The modeling approach is proposed for application in three dimensional models of cardiovascular stenting procedures.

Multi-scale modelling of arterial tissue: Linking networks of fibres to continua

2018 ◽  
Vol 341 ◽  
pp. 740-787
Author(s):  
Felipe Figueredo Rocha ◽  
Pablo Javier Blanco ◽  
Pablo Javier Sánchez ◽  
Raúl Antonino Feijóo
Keyword(s):  
Multi Scale ◽  
Arterial Tissue ◽  
Scale Modelling

Differential modulation of caffeine- and IP3-induced calcium release in cultured arterial tissue

1999 ◽  
Vol 276 (5) ◽  
pp. C1115-C1120 ◽  
Author(s):  
Karl Dreja ◽  
Per Hellstrand
Keyword(s):  
Calcium Release ◽  
Cyclopiazonic Acid ◽  
Differential Modulation ◽  
Transient Responses ◽  
Inositol 1,4,5 Trisphosphate ◽  
Arterial Tissue ◽  
Intracellular Ca ◽  
Rat Tail

To investigate the Ca2+-dependent plasticity of sarcoplasmic reticulum (SR) function in vascular smooth muscle, transient responses to agents releasing intracellular Ca2+ by either ryanodine (caffeine) ord- myo-inositol 1,4,5-trisphosphate [IP3; produced in response to norepinephrine (NE), 5-hydroxytryptamine (5-HT), arginine vasopressin (AVP)] receptors in rat tail arterial rings were evaluated after 4 days of organ culture. Force transients induced by all agents were increased compared with those induced in fresh rings. Stimulation by 10% FCS during culture further potentiated the force and Ca2+ responses to caffeine (20 mM) but not to NE (10 μM), 5-HT (10 μM), or AVP (0.1 μM). The effect was persistent, and SR capacity was not altered after reversible depletion of stores with cyclopiazonic acid. The effects of serum could be mimicked by culture in depolarizing medium (30 mM K+) and blocked by the addition of verapamil (1 μM) or EGTA (1 mM) to the medium, lowering intracellular Ca2+ concentration ([Ca2+]i) during culture. These results show that modulation of SR function can occur in vitro by a mechanism dependent on long-term levels of basal [Ca2+]iand involving ryanodine- but not IP3 receptor-mediated Ca2+release.

Insensitivity to insulin of human arterial tissue in vitro

1979 ◽  
Vol 106 (4) ◽  
pp. 493-494 ◽  
Author(s):  
H. J. ARNQVIST ◽  
R. BERGLIND ◽  
H. H. DAHLKVIST ◽  
E. VARENHORST
Keyword(s):  
Arterial Tissue
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