scholarly journals Histopathological study on serial changes in anastomosed carotid artery in rats; with special reference to intimal hyperplasia and re-endothelialization.

Nosotchu ◽  
1991 ◽  
Vol 13 (6) ◽  
pp. 613-628
Author(s):  
Tomoko Morita ◽  
Masahiro Kurisaka ◽  
Koreaki Mori ◽  
Hiroshi Sonobe ◽  
Yuji Ohtsuki
Circulation ◽  
1995 ◽  
Vol 91 (11) ◽  
pp. 2793-2801 ◽  
Author(s):  
Takayuki Asahara ◽  
Christophe Bauters ◽  
Christopher Pastore ◽  
Marianne Kearney ◽  
Susan Rossow ◽  
...  

2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
John T Favreau ◽  
Chengwei Liu ◽  
Peng Yu ◽  
Christine Mauro ◽  
Ming Tao ◽  
...  

Intimal hyperplasia (IH) remains the major culprit in revascularization failures. We aimed to unravel relationships between acute changes in circumferential arterial wall strain and genesis of IH. Methods To induce IH, we employed a validated model using a 9-0 nylon suture tie around the distal mouse common carotid artery (n=10) and an external 35-gauge needle mandrel (OD=0.14mm), with subsequent removal of the mandrel to create a distal common carotid focal stenosis (~78% lumen diameter/~85% flow reduction). Wall strains were measured in three, 1 mm wide regions along the vessel proximal to the focal stenosis at pre-op day 1 and at post-op day 4 (before detectable IH) using Vevo 2100 ultrasonography with VevoVasc software. At post-op day 28, arteries were perfusion fixed and IH was assessed in the same regions as those where strain was analyzed. Strain and morphology were also assessed in the contralateral control artery. Results Decreased wall strain was noted in all regions proximal to the focal stenosis from 0.26 ± 0.01 to 0.11 ± 0.02 (p<0.001) with no change in the control artery from pre-op to post-op day 4 (p=0.45). Based on a strain level histogram, vessels were divided into groups with strain ≤0.1 and >0.1. All segments (n = 13) with wall strain ≤0.1 at post-op day 4 had significant IH at day 28. In regions with strains >0.1 at day 4, only 30% had IH at day 28. The average pre-op strains were identical in >0.1 and ≤0.1 strain groups (0.27 ± 0.09 and 0.27 ± 0.08). Mean intimal thickness in vessels with strain ≤0.1 was 32 ± 20 μm, significantly greater than 8.0 ± 16 μm in the group with strain >0.1 (p<0.01). To further understand the mechanisms underlying changes in strain, systolic and diastolic lumen areas were assessed. Although systolic lumen areas in both >0.1 and ≤0.1 groups remained unchanged from pre-op to post-op day 4 (p=0.46), diastolic area was significantly increased in regions with post-op day 4 strain ≤0.1 (p=0.04) but remained unchanged in mice with post-op day 4 strain >0.1 (p=0.67). Conclusions Acute reduction in wall strain precedes the formation of IH in this murine model and this change is primarily caused by an increase in diastolic lumen area. Manipulations of wall strain offer a strategy to prevent and attenuate occlusive IH lesions after revascularizations.


2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
He Shuying ◽  
Wu Jie

To determine the effects of heparin-derived oligosaccharides (HDOs) on vascular intimal hyperplasia (IH) in balloon-injured carotid artery and the mechanism involved. The animal model was established by rubbing the endothelia within the common carotid artery (CCA) of male rabbits along with a high-cholesterol diet. The arterial IH was testified by histopathological changes of the CCA. Serum lipids were detected using automated biochemical analysis; Expression of mRNAs corresponding to vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), vascular cell adhesion molecule-1 (VCAM-1), monocyte chemoattractant protein-1 (MCP-1), scavenger receptor class B type I (SR-BI) and ATP-binding cassette transporter A1 (ABCA-1) were analyzed using reverse transcription polymerase chain reaction assays. Expressions of VEGF, VCAM-1, MCP-1, SR-BI and ABCA-1 proteins were detected by western blotting. Enzyme-linked immunosorbent assays were used to quantify expression levels of VEGF and bFGF. The results implied that administration of HDO significantly inhibited common carotid artery histopathology and restenosis that was induced by balloon injury. Treatment with HDO also significantly decreased mRNA and protein expression levels of VEGF, bFGF, VCAM-1, MCP-1, and SR-BI in the arterial wall, however ABCA-1 expression levels were elevated. HDO treatment led to a reduction in various serum lipids (total cholesterol, triglycerides, high-density and low-density lipoproteins). We concluded that, in a rabbit model, HDO can ameliorate IH and the mechanisms might involved VEGF, bFGF, VCAM-1, MCP-1, SR-BI and ABCA-1.


2000 ◽  
Vol 82 ◽  
pp. 191
Author(s):  
Tomoko Ishibashi ◽  
Satoshi Obayashi ◽  
Takeshi Aso ◽  
Hiroshi Azuma

Surgery Today ◽  
2002 ◽  
Vol 32 (7) ◽  
pp. 618-622 ◽  
Author(s):  
Masafumi Akita ◽  
Hiroaki Takenaka ◽  
Masakazu Harada ◽  
Tao-Sheng Li ◽  
Hua Zhang ◽  
...  

2002 ◽  
Vol 3 (1) ◽  
pp. 16-19 ◽  
Author(s):  
David Rosenthal ◽  
Scott L Stevens ◽  
C.S Skillern ◽  
Eric D Wellons ◽  
Keith Robinson ◽  
...  

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