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Autor     Matthias Heil, Wolfgang Schaper
Titel    Influence of Mechanical, Cellular, and Molecular Factors on Collateral Artery Growth (Arteriogenesis)
Zeitschrift    Circulation Research
Ausgabe    95
Jahr    2004
Seiten    449-458
ISSN    1524-4571
DOI    10.1161/01.RES.0000141145.78900.44
URL    http://circres.ahajournals.org/content/95/5/449.full.pdf

Literaturverz.   

ja
Fußnoten    ja
Fragmente    5


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[1.] Haw/Fragment 003 04 - Diskussion
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Quelle: Heil and Schaper 2004
Seite(n): 449, Zeilen: Abstract
Growth of collateral blood vessels (arteriogenesis) is potentially able to preserve structure and function of limbs and organs after occlusion of a major artery. The success of the remodeling process depends on the following conditions: (1) existence of an arteriolar network that connects the preocclusive with the postocclusive microcirculation; (2) activation of the arteriolar endothelium by elevated fluid shear stress; (3) invasion (but not incorporation) of bone marrow–derived cells; and (4) proliferation of endothelial and smooth muscle cells[9].

9. Heil, M. and W. Schaper, Influence of mechanical, cellular, and molecular factors on collateral artery growth (arteriogenesis). Circ Res, 2004. 95(5): p. 449-58.

Growth of collateral blood vessels (arteriogenesis) is potentially able to preserve structure and function of limbs and organs after occlusion of a major artery. The success of the remodeling process depends on the following conditions: (1) existence of an arteriolar network that connects the preocclusive with the postocclusive microcirculation; (2) activation of the arteriolar endothelium by elevated fluid shear stress; (3) invasion (but not incorporation) of bone marrow–derived cells; and (4) proliferation of endothelial and smooth muscle cells.
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[2.] Haw/Fragment 003 27 - Diskussion
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Mature collateral vessels differ only in minor histological aspects from normal arteries of the conductance type: they are muscular and contain more collagen and exhibit transiently, during the growth process, a significant intima consisting of smooth muscle cells in the synthetic and proliferative phenotype. Mature collateral vessels differ only in minor histological aspects from normal arteries of the conductance type: they are muscular and contain more collagen and exhibited transiently during the growth process a significant intima consisting of smooth muscle cells in the synthetic and proliferative phenotype.
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[3.] Haw/Fragment 004 01 - Diskussion
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[However, they differ markedly in their] anatomical appearance: they are sometimes excessively tortuous[13, 25]. In the re-entry region, they join up with the distal part of the occluded artery at nonphysiological angles, which adds to the resistance to flow. Collateral arteries can develop relatively quickly provided a pre-existent network of arterioles had existed before occlusion of the artery but they can also quickly regress when the occluded artery is opened up again[22]. This may also be the case when the subtended tissue had atrophied or is not used to full potential like in the peripheral circulation supplying the muscles of the leg. Most often, an occluded artery is not replaced by one single large collateral vessel but rather by several smaller ones. But this arrangement is inefficient because according to the Poiseuille’s Law the energy losses created by the resistance of the contributing vessels are additive[9]. During the course of collateral artery development many of the smaller contributing vessels regress, whereas the larger ones increase in diameter and make the system more efficient. However, no ideal adaptation is reached. At optimal conditions (no tissue loss after arterial occlusion), collateral vessels recover only approximately 40% of the maximal conductance (flow at a given blood pressure at maximal vasodilatation). This was shown for the canine heart and for the peripheral circulation in pigs, rabbits, and mice[7, 26].

7. Ito, W.D., et al., Angiogenesis but not collateral growth is associated with ischemia after femoral artery occlusion. Am J Physiol, 1997. 273(3 Pt 2): p. H1255-65.

9. Heil, M. and W. Schaper, Influence of mechanical, cellular, and molecular factors on collateral artery growth (arteriogenesis). Circ Res, 2004. 95(5): p. 449-58.

13. Schaper, W., Tangential wall stress as a molding force in the development of collateral vessels in the canine heart. Experientia, 1967. 23(7): p. 595-6.

22. Fulton, W.F., The Time Factor in the Enlargement of Anastomoses in Coronary Artery Disease. Scott Med J, 1964. 9: p. 18-23.

25. Korff, T., K. Aufgebauer, and M. Hecker, Cyclic stretch controls the expression of CD40 in endothelial cells by changing their transforming growth factor-beta1 response. Circulation, 2007. 116(20): p. 2288-97.

26. Kumada, T., et al., Comparison of postpacing and exercise-induced myocardial dysfunction during collateral development in conscious dogs. Circulation, 1982. 65(6): p. 1178-85.

However, they differ markedly in their anatomical appearance: they are sometimes excessively tortuous.1 In the reentry region, they join up with the distal part of the occluded artery at nonphysiological angles, which adds to the resistance toward flow. Collateral arteries can develop relatively quickly provided a preexistent network of arterioles had existed before occlusion of the artery but they can also quickly regress when the occluded artery is opened up again.2 This may also be the case when the subtended tissue had atrophied or is not used to full potential like in the peripheral circulation supplying the muscles of the leg. Most often, an occluded artery is not replaced by one single large collateral vessel but rather by several smaller ones. But this arrangement is inefficient because according to the Poiseuille’s Law the energy losses created by the resistance of the contributing vessels are additive. During the course of collateral artery development many of the smaller contributing vessels regress, whereas the larger ones increase in diameter and make the system more efficient. However, no ideal adaptation is reached. At optimal conditions (no tissue loss after arterial occlusion), collateral vessels recover only approximately 40% of the maximal conductance (flow at a given blood pressure at maximal vasodilatation). This was shown for the canine heart and for the peripheral circulation in pigs, rabbits, and mice.3–5

1. Schaper W. The Collateral Circulation of the Heart. Amsterdam London: Elsevier North Holland Publishing Company; 1971.

2. Fulton WFM. The time factor in the enlargement of anastomoses in coronary artery disease. Scot Med J. 1964;9:18–23.

3. Kumada T, Gallagher KP, Battler A, White F, Kemper WS, Ross Jr J. Comparison of postpacing and exercise-induced myocardial dysfunction during collateral development in conscious dogs. Circulation. 1982;65:1178–1185.

4. Ito WD, Arras M, Scholz D, Winkler B, Htun P, Schaper W. Angiogenesis but not collateral growth is associated with ischemia after femoral artery occlusion. Am J Physiol. 1997;273:H1255–H1265.

5. Elsaesser H, Sauer A, Friedrich C, Helisch A, Luttun A, Carmeliet P, Scholz D, Schaper W. Bone marrow transplants abolish inhibition of arteriogenesis in placenta growth factor k.o. mice. J Mol Cell Cardiol. 2000;32:A29. Abstract

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[4.] Haw/Fragment 004 25 - Diskussion
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The collateral vessel wall is now exposed to various pronounced mechanical forces: increased blood flow directly augments FSS, i.e., the viscous drag that flowing blood exerts on the endothelial lining. Assuming Newtonian fluid dynamics, FSS can be estimated using the following equation: Hence, the collateral vessel wall is now exposed to various pronounced mechanical forces: increased blood flow directly augments fluid shear stress (FSS), ie, the viscous drag that flowing blood exerts on the endothelial lining. Assuming Newtonian fluid dynamics, FSS can be estimated using the following equation:
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The equation that already includes blood viscosity (η) and the internal radius of a vessel (R), demonstrates that increased blood flow (Q) will directly result in increased FSS (τ)[9]. Furthermore, the wall of the collateral arteriole is influenced by pressure-related forces like longitudinal-, circumferential-, and radial wall stresses.


9. Heil, M. and W. Schaper, Influence of mechanical, cellular, and molecular factors on collateral artery growth (arteriogenesis). Circ Res, 2004. 95(5): p. 449-58.

Haw 05a source.png

The equation that already includes blood viscosity (η) and the internal radius of a vessel (R), demonstrates that increased blood flow (Q) will directly result in increased FSS (τ).8 Furthermore, the wall of the collateral arteriole is influenced by pressure-related forces like longitudinal-, circumferential-, and radial wall stresses.


8. Cox R. Physiology and hemodynamics of the macrocirculation. In: Stehbens W, eds. Hemodynamics and the Blood Vessel Wall. Springfield, Ill: Charles C. Thomas; 1979:75–156.

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