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Typus
BauernOpfer
Bearbeiter
Hindemith
Gesichtet
Yes.png
Untersuchte Arbeit:
Seite: 4, Zeilen: 1-17
Quelle: Heil and Schaper 2004
Seite(n): 450, Zeilen: l. Spalte: 11ff
[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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