Contribution of Arteriogenesis and Angiogenesis to Postocclusive Hindlimb Perfusion in Mice

Scholz, Dimitri; Ziegelhoeffer, Tibor; Helisch, Armin; Wagner, Shawn; Friedrich, Christian; Podzuweit, Thomas; Schäper, Wolfgang

doi:10.1006/jmcc.2002.2013

Cited by 319 publications

(405 citation statements)

References 23 publications

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“…That capillary sprouting is able to reduce minimal resistance was shown by us previously in the pig heart. 20 We had also shown previously that ischemia is not a requirement for arteriogenesis from experiments in the rabbit 10,21 and mouse hind leg. We therefore conclude that also under the conditions of venous drainage of collateral flow, ischemia had not influenced the development of collateral vessels in the upper leg.…”

Section: Alternative Explanationsmentioning

confidence: 52%

Elevated Fluid Shear Stress Enhances Postocclusive Collateral Artery Growth and Gene Expression in the Pig Hind Limb

Pipp

Boehm

Cai

et al. 2004

ATVB

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212

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Objective-The role of fluid shear stress (FSS) in collateral vessel growth remains disputed and prospective in vivo experiments to test its morphogenic power are rare. Therefore, we studied the influence of FSS on arteriogenesis in a new model with extremely high levels of collateral flow and FSS in pig and rabbit hind limbs. Methods and Results-A side-to-side anastomosis was created between the distal stump of one of the bilaterally occluded femoral arteries with the accompanying vein. This clamps the collateral reentry pressure at venous levels and increases collateral flow, which is directed to a large part into the venous system. This decreases circumferential wall stress and markedly increases FSS. One week after anastomosis, angiographic number and size of collaterals were significantly increased. Maximal collateral flow exceeded by 2.3-fold that obtained in the ligature-only hind limb. Capillary density increased in lower leg muscles. Immunohistochemistry revealed augmented proliferative activity of endothelial and smooth muscle cells. Intercellular adhesion molecule-1 and vascular cell adhesion molecule (VCAM)-1 were upregulated, and monocyte invasion was markedly increased. In 2-dimensional gels, actin-regulating cofilin1 and cofilin2, destrin, and transgelin2 showed the highest degree of differential regulation. Conclusions-High levels of FSS cause a strong arteriogenic response, reinstate cellular proliferation, stimulate cytoskeletal rearrangement, and normalize maximal conductance. FSS is the initiating molding force in arteriogenesis. Key Words: fluid shear stress Ⅲ shunt Ⅲ arteriogenesis Ⅲ proteomics Ⅲ cytoskeletal proteins N umerous studies have documented the influence of fluid shear stress (FSS) as an arterial molding force, 1-3 but information on the actions of markedly increased in vivo FSS on the development of arterial collateral vessels after occlusion of a conduit artery is lacking. Such studies are needed because attempts at changing FSS often also alter the circumferential wall stress, another acknowledged molding force of growing collateral vessels. The formation of a collateral circulation after an arterial occlusion correlates well with the calculated increase in FSS because of the increased collateral flow caused by the pressure decrease along pre-existent collaterals. However, because of the fast increase in collateral diameter by cellular proliferation, FSS decreases quickly again, and the early termination of the growth process at an incomplete stage of adaptation is believed to be caused by the only transient action of FSS. One of the hypotheses to be tested was, therefore, whether prolonged action of FSS would also improve the final adaptation by continued growth. The present experiments were therefore undertaken to prospectively study the causal relations between arteriogenesis and FSS by a stepwise and lasting increase of collateral flow brought about by the creation of a side-to-side anastomosis between the distal stump of the occluded femoral artery and its accompanying vei...

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Section: Alternative Explanationsmentioning

confidence: 52%

Elevated Fluid Shear Stress Enhances Postocclusive Collateral Artery Growth and Gene Expression in the Pig Hind Limb

Pipp

Boehm

Cai

et al. 2004

ATVB

Self Cite

212

197

View full text Add to dashboard Cite

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“…As this occlusion will be permanent, chronic increases in wall shear stress will also be relevant to physiological recovery from the ligation surgery. As previously stated long lasting increases in shear wall stress induce arteriogenesis (refer back to Figure 5) [30,32,33].…”

Section: Femoral Artery Ligation Modelsupporting

confidence: 63%

“…Based on the aforementioned data it appears (based on previous research) that collateralization of the muscular branch was induced by the femoral artery ligation conditions (primarily high shear stress, normoxia and likely mild inflammation) [32].…”

Section: Vasodilation In Arteriogenic Conditions (Femoral Artery Ligamentioning

confidence: 97%

“…Collateralization describes the outward remodeling of linked arterioles into conduit arteries [31]. Chronic increases in shear stress have been demonstrated to induce arteriole growth and outward remodeling [32].…”

Section: Arteriogenesismentioning

confidence: 99%

“…Thus there appeared to be a slight but not significant decrease in the luminal diameter of the muscular branch following femoral artery resection and subsequent revascularization after 2 weeks. Previous studies have stressed the importance of shear stress in the induction of outward remodeling [30,32,33]. This would imply that since there was neutral arterial remodeling that there was no increase in shear stress or blood flow following the ischemic insult.…”

Section: Remodeling Following Non-arteriogenic Ischemiamentioning

confidence: 99%

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Arteriogenic Revascularization Does Not Induce Vascular Function Impairment

Yocum¹

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Arteriogenic Revascularization Does Not Induce Vascular Function Impairment Matthew YocumFunctional hyperemia and arteriolar vasodilation are impaired with chronic ischemia. We sought to examine the impact of chronic ischemia on collateral artery function. For this we used two hindlimb ischemia models to dissect the impact of different repair processes on collateral function. Ligation of the femoral artery increases shear stress in the muscular branch and results in outward remodeling and arteriogenesis. In contrast, resection of the femoral artery proximal to the muscular branch induces blood flow divergence and neutral remodeling along with expectedly greater hypoxia and inflammation. On day 14 after each surgery the diameter of the muscular branch was measured using sidestream dark field (SDF) imaging before and after gracilis muscle stimulation. A slight, but not statistically significant, impairment in functional vasodilation was observed in ligated mice (69±10% average diameter increase compared to 74±7% average diameter increase). Resected mice exhibited slightly (not statistically significant) enhanced collateral artery functional vasodilation (104±16% average diameter increase) but were also refractory to the restoration of resting vascular tone following the cessation of stimulation. Outward remodeling did not significantly impair vascular function, whereas neutral remodeling and tissue hypoxia induced impaired vascular tone.

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Therapeutic Angiogenesis

Gerritsen¹

2006

Encyclopedia of Molecular Cell Biology and Molecular Medicine

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Contribution of Arteriogenesis and Angiogenesis to Postocclusive Hindlimb Perfusion in Mice

Cited by 319 publications

References 23 publications

Elevated Fluid Shear Stress Enhances Postocclusive Collateral Artery Growth and Gene Expression in the Pig Hind Limb

Elevated Fluid Shear Stress Enhances Postocclusive Collateral Artery Growth and Gene Expression in the Pig Hind Limb

Arteriogenic Revascularization Does Not Induce Vascular Function Impairment

Therapeutic Angiogenesis

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