Myointimal Hyperplasia: Pathogenesis and Implications. 2. Animal Injury Models and Mechanical Factors

Painter, T.A.

doi:10.1111/j.1525-1594.1991.tb00768.x

Cited by 38 publications

(6 citation statements)

References 129 publications

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“…Re-occlusion often occurs due to neointimal hyperplasia, when vascular smooth muscle cells (VSMCs) over-proliferate, migrate inward and choke off the blood flow (2, 3). In general, this process is initiated by endothelial injury and subsides as the endothelium heals (4). In addition, stenosis sites are often very small and local (5), while the remaining length of vessel experiences little to no lumenal narrowing (6).…”

Section: Introductionmentioning

confidence: 99%

Endothelial Injury Induces Vascular Smooth Muscle Cell Proliferation in Highly Localized Regions of a Direct Contact Co-culture System

Jacot

Wong

2008

Cell Biochem Biophys

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Though previous studies have indicated a relationship between the proliferation of endothelial cells and vascular smooth muscle cells (VSMCs) in co-culture, the results have been contradictory and the signaling mechanism poorly understood. In this transmembrane co-culture study, VSMCs and endothelial cells were grown to confluence on opposite sides of a microporous membrane to mimic the intima/media border of vessels. The endothelial layer was injured, and then cultured for three days, resulting in partial re-endothelialization. VSMC proliferation across from the injured/partially recovered endothelial region was significantly higher than across from the de-endothelialized region (a 7-fold increase) and the uninjured region (a 3-fold increase). ELISA indicated that PDGF, which was undetectable in uninjured co-culture and homotypic controls, increased after injury and the addition of a piperazinylquinazoline carboxamide PDGF receptor inhibitor blocked VSMC proliferation across from the injured/partially recovered region. We conclude that co-culture signaling initiated by endothelial cell injury locally stimulates VSMC proliferation and that this signaling could be mediated by PDGF-BB.

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Section: Introductionmentioning

confidence: 99%

Endothelial Injury Induces Vascular Smooth Muscle Cell Proliferation in Highly Localized Regions of a Direct Contact Co-culture System

Jacot

Wong

2008

Cell Biochem Biophys

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“…There are some major differences between the models. For example, the observation time in the myointimal hyperplasia model is 28 days 16 , while atherosclerotic plaque development needs four to six months 17 …”

Section: Discussionmentioning

confidence: 99%

“…Now the intestines can be arranged back in situ. 16. Rinse the abdominal cavity utilizing pre-warmed sterile saline.…”

Section: Myointimal Hyperplasia Model (A)mentioning

confidence: 99%

Inducing Myointimal Hyperplasia Versus Atherosclerosis in Mice: An Introduction of Two Valid Models

Stubbendorff

Hua

Deuse

et al. 2014

JoVE

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Various in vivo laboratory rodent models for the induction of artery stenosis have been established to mimic diseases that include arterial plaque formation and stenosis, as observed for example in ischemic heart disease. Two highly reproducible mouse models -both resulting in artery stenosis but each underlying a different pathway of development -are introduced here. The models represent the two most common causes of artery stenosis; namely one mouse model for each myointimal hyperplasia, and atherosclerosis are shown. To induce myointimal hyperplasia, a balloon catheter injury of the abdominal aorta is performed. For the development of atherosclerotic plaque, the ApoE -/-mouse model in combination with western fatty diet is used. Different model-adapted options for the measurement and evaluation of the results are named and described in this manuscript. The introduction and comparison of these two models provides information for scientists to choose the appropriate artery stenosis model in accordance to the scientific question asked. Video LinkThe video component of this article can be found at

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“…The responsible factors for synthetic graft failure may be listed as follows [8,[14][15][16][17] : (1) mechanical factors which include compliance mismatch between flexible native arteries and stiff graft walls, graft's size (diameter), failure of the graft material itself, surgical technique (anastomosis shape, anastomosis type, suture technique, suture material, distal run-off, etc. ); (2) biological factors which include blood contact with the non-endothelialized graft surface, inducing thrombosis, infection, trauma and inflammation at the anastomoses and intimal hyperplasia reaction.…”

Section: Discussionmentioning

confidence: 99%

Matching the Diameter of ePTFE Bypass Prosthesis with a Native Artery Improves Neoendothelialization

Çıkırıkçıoğlu

Pektok²,

Cikirikcioglu³

et al. 2008

Eur Surg Res

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Background and Aim: The undersizing of the bypass graft diameter compared to native artery changes blood flow characteristics and velocity which may affect conduit neo-endothelialization, intimal hyperplasia reaction and patency. The aim of this study was to evaluate conduit neoendothelialization, intimal hyperplasia reaction and patency results between undersized and matched ePTFE grafts. Material and Methods: In 16 male Sprague-Dawley rats, undersized (1-mm internal diameter) and matched (2-mm internal diameter) ePTFE grafts were anastomosed end-to-end in the infrarenal abdominal aorta. Blood flow volume per minute was measured and wall shear stress was calculated for each group. After 3 weeks of follow-up, angiography was performed via the left carotid artery just before sacrifice. Conduit neoendothelialization and intimal hyperplasia reaction were measured by computer-assisted morphometry. Results: Wall shear stress was 8 times higher for the undersized group (840.56 vs. 105.07 mPa). Three weeks after implantation, conduit neoendothelialization was better in matched grafts compared to undersized grafts (441 vs. 574 µm, p = 0.008). Intimal hyperplasia reaction was similar for both groups (8.7 vs. 6.7 µm²/µm for undersized and matched grafts, respectively). Patency rate was 7/8 for undersized and 8/8 for matched ePTFE grafts. Conclusion: Although the graft patency and the intimal hyperplasia reaction were not different between the two groups after 3 weeks, matched grafts had a significantly better endothelialization compared to undersized grafts. This short-term beneficial effect may influence long-term patency results.

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Myointimal Hyperplasia: Pathogenesis and Implications. 2. Animal Injury Models and Mechanical Factors

Abstract: Vasko JS. Intimal changes in arteriovenous bypass grafts. Effects of varying the angle of implantation at the proximal anastomosis end on producing stenosis in the distal runoff artery.

Cited by 38 publications

References 129 publications

Endothelial Injury Induces Vascular Smooth Muscle Cell Proliferation in Highly Localized Regions of a Direct Contact Co-culture System

Endothelial Injury Induces Vascular Smooth Muscle Cell Proliferation in Highly Localized Regions of a Direct Contact Co-culture System

Inducing Myointimal Hyperplasia Versus Atherosclerosis in Mice: An Introduction of Two Valid Models

Matching the Diameter of ePTFE Bypass Prosthesis with a Native Artery Improves Neoendothelialization

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