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Angaben zur Quelle [Bearbeiten]

Autor     Wolfgang Schaper
Titel    Collateral circulation Past and present
Zeitschrift    Basic Research in Cardiology
Verlag    Springer
Ausgabe    104
Jahr    2009
Seiten    5-21
DOI    10.1007/s00395-008-0760-x
URL    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2755790/pdf/395_2008_Article_760.pdf

Literaturverz.   

ja
Fußnoten    ja
Fragmente    2


Fragmente der Quelle:
[1.] Haw/Fragment 005 06 - Diskussion
Zuletzt bearbeitet: 2014-10-16 17:55:23 Singulus
BauernOpfer, Fragment, Gesichtet, Haw, SMWFragment, Schaper 2009, Schutzlevel sysop

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Hindemith
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Untersuchte Arbeit:
Seite: 5, Zeilen: 6-12
Quelle: Schaper 2009
Seite(n): 7, Zeilen: r. Spalte: 15ff
It is generally assumed that a physical stimulus starts the remodeling process whereby increased pressure leads to increased wall thickness and increased flow to increased arterial diameter. Pressure-dependent forces are by far the highest in magnitude and they affect both the endothelium as well as the muscular media. It is therefore logical to assume that these are important factors for remodeling[13, 25]. However, in collateral growth with its pressure gradient driven increase in flow, the much weaker FSS, which the viscous drag of flowing blood exerts on the endothelial [lining, is the determining force[11, 29-35].]

11. Eitenmuller, I., et al., The range of adaptation by collateral vessels after femoral artery occlusion. Circ Res, 2006. 99(6): p. 656-62.

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.

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.

29. Ben Driss, A., et al., Arterial expansive remodeling induced by high flow rates. Am J Physiol, 1997. 272(2 Pt 2): p. H851-8.

30. Buus, C.L., et al., Smooth muscle cell changes during flow-related remodeling of rat mesenteric resistance arteries. Circ Res, 2001. 89(2): p. 180-6.

31. Girard, P.R. and R.M. Nerem, Shear stress modulates endothelial cell morphology and F-actin organization through the regulation of focal adhesion-associated proteins. J Cell Physiol, 1995. 163(1): p. 179-93.

32. Langille, B.L., Remodeling of developing and mature arteries: endothelium, smooth muscle, and matrix. J Cardiovasc Pharmacol, 1993. 21 Suppl 1: p. S11-7.

33. Resnick, N., et al., Fluid shear stress and the vascular endothelium: for better and for worse. Prog Biophys Mol Biol, 2003. 81(3): p. 177-99.

34. Tronc, F., et al., Role of NO in flow-induced remodeling of the rabbit common carotid artery. Arterioscler Thromb Vasc Biol, 1996. 16(10): p. 1256-62.

35. Tzima, E., et al., A mechanosensory complex that mediates the endothelial cell response to fluid shear stress. Nature, 2005. 437(7057): p. 426-31.

It is generally assumed that a physical stimulus starts the remodeling process whereby increased pressure leads to increased wall thickness and increased flow to increased arterial diameter. Pressure-dependent forces are by far the highest in magnitude and they affect both the endothelium as well as the muscular media. It is therefore logical to assume that these are important factors for remodeling [83, 121, 122]. [...] However, in collateral growth with its pressure gradient driven increase in flow the much weaker FSS, which the viscous drag of flowing blood exerts on the endothelial lining, is the determining force [8, 17, 35, 49, 85, 114, 142, 145, 149].

8. Ben Driss A, Benessiano J, Poitevin P, Levy BI, Michel JB (1997) Arterial expansive remodeling induced by high flow rates. Am J Physiol 272:H851–H858

17. Buus CL, Pourageaud F, Fazzi GE, Janssen G, Mulvany MJ, De Mey JG (2001) Smooth muscle cell changes during flow-related remodeling of rat mesenteric resistance arteries. Circ Res 89:180–186

35. Eitenmuller I, Volger O, Kluge A, Troidl K, Barancik M, Cai WJ, Heil M, Pipp F, Fischer S, Horrevoets AJ, Schmitz-Rixen T, Schaper W (2006) The range of adaptation by collateral vessels after femoral artery occlusion. Circ Res 99:656–662

49. Girard PR, Nerem RM (1995) Shear stress modulates endothelial cell morphology and F-actin organization through the regulation of focal adhesion- associated proteins. J Cell Physiol 163:179–193

83. Korff T, Aufgebauer K, Hecker M (2007) Cyclic stretch controls the expression of CD40 in endothelial cells by changing their transforming growth factor-beta1 response. Circulation 116:2288–2297

85. Langille BL (1993) Remodeling of developing and mature arteries: endothelium, smooth muscle, and matrix. J Cardiovasc Pharmacol 21(Suppl 1):S11–S17

114. Resnick N, Yahav H, Shay-Salit A, Shushy M, Schubert S, Zilberman LC, Wofovitz E (2003) Fluid shear stress and the vascular endothelium: for better and for worse. Prog Biophys Mol Biol 81:177–199

121. Schaper W (1967) Tangential wall stress as a molding force in the development of collateral vessels in the canine heart. Experientia 23:595– 596

122. Schaper W (1971) The collateral circulation of the heart. Elsevier North Holland Publishing Company, Amsterdam

142. Thoma R (1893) Untersuchungen über die Histogenese und Histomechanik des Gefäßsystems. F.Enke, Stuttgart

145. Tronc F, Wassef M, Esposito B, Henrion D, Glagov S, Tedgui A (1996) Role of NO in flow-induced remodeling of the rabbit common carotid artery. Arterioscler Thromb Vasc Biol 16:1256–1262

149. Tzima E, Irani-Tehrani M, Kiosses WB, Dejana E, Schultz DA, Engelhardt B, Cao G, DeLisser H, Schwartz MA (2005) A mechanosensory complex that mediates the endothelial cell response to fluid shear stress. Nature 437:426–431

Anmerkungen

Ein Verweis auf die Quelle folgt auf der nächsten Seite.

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[2.] Haw/Fragment 006 01 - Diskussion
Zuletzt bearbeitet: 2014-10-16 17:57:41 Singulus
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Untersuchte Arbeit:
Seite: 6, Zeilen: 1-9
Quelle: Schaper 2009
Seite(n): 7, Zeilen: r. Spalte: 33ff
The pressure derived pulsatile stretch is also discussed[25, 36, 37], and the transcription factor- activator protein 1 (AP-1) is the molecular transducer. However, AP-1 is also activated by FSS[38], Pulsatile stretch can only be tested acutely and in vitro with its inherent limits. Cultured endothelium under stretch alters translation and transcription of growth factors and changes the sensitivity to cytokines[11, 39, 40]. If pulsatile stretch is a molding force, it must be demonstrated that in collateral growth pulsatile stretch is higher than the physiological levels in normal small arteries. Furthermore, in arterial occlusion the intravascular pressure downstream from the occlusion is much lower than the systemic arterial pressure[8].

8. Schaper, W., Collateral circulation: past and present. Basic Res Cardiol, 2009. 104(1): p. 5-21.

11. Eitenmuller, I., et al., The range of adaptation by collateral vessels after femoral artery occlusion. Circ Res, 2006. 99(6): p. 656-62.

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.

36. Lehoux, S., et al., Differential regulation of vascular focal adhesion kinase by steady stretch and pulsatility. Circulation, 2005. 111(5): p. 643-9.

37. Popp, R., I. Fleming, and R. Busse, Pulsatile stretch in coronary arteries elicits release of endothelium-derived hyperpolarizing factor: a modulator of arterial compliance. Circ Res, 1998. 82(6): p. 696-703.

38. Miyagi, M., et al., Activator protein-1 mediates shear stress-induced prostaglandin d synthase gene expression in vascular endothelial cells. Arterioscler Thromb Vasc Biol, 2005. 25(5): p. 970-5.

39. Busse, R. and I. Fleming, Pulsatile stretch and shear stress: physical stimuli determining the production of endothelium-derived relaxing factors. J Vasc Res, 1998. 35(2): p. 73-84.

40. Demicheva, E., M. Hecker, and T. Korff, Stretch-induced activation of the transcription factor activator protein-1 controls monocyte chemoattractant protein-1 expression during arteriogenesis. Circ Res, 2008. 103(5): p. 477-84.

However, pressure derived pulsatile stretch is also discussed [83, 88, 110] and the transcription factor AP-1 is the molecular transducer. However, AP-1 is also activated by FSS [96]. Pulsatile stretch can only be tested acutely and in vitro with its inherent limits. Cultured endothelium under stretch alters translation and transcription of growth factors and changes the sensitivity to cytokines[14, 32, 110]. If pulsatile stretch is a molding force it must be demonstrated that in collateral growth pulsatile stretch is higher than the physiological levels in normal small arteries. Furthermore, in arterial occlusion the intravascular pressure downstream from the occlusion (and hence in the receiving end of the collateral arcade) is much lower than the systemic arterial pressure [...]

14. Busse R, Fleming I (1998) Pulsatile stretch and shear stress: physical stimuli determining the production of endothelium-derived relaxing factors. J Vasc Res 35:73–84

32. Demicheva E, Hecker M, Korff T (2008) Stretch-induced activation of the transcription factor activator protein-1 controls monocyte chemoattractant protein-1 expression during arteriogenesis. Circ Res (in press)

83. Korff T, Aufgebauer K, Hecker M (2007) Cyclic stretch controls the expression of CD40 in endothelial cells by changing their transforming growth factor-beta1 response. Circulation 116:2288–2297

88. Lehoux S, Esposito B, Merval R, Tedgui A (2005) Differential regulation of vascular focal adhesion kinase by steady stretch and pulsatility. Circulation 111:643–649

96. Miyagi M, Miwa Y, Takahashi-Yanaga F, Morimoto S, Sasaguri T (2005) Activator protein-1 mediates shear stress-induced prostaglandin d synthase gene expression in vascular endothelial cells. Arterioscler Thromb Vasc Biol 25:970–975

110. Popp R, Fleming I, Busse R (1998) Pulsatile stretch in coronary arteries elicits release of endothelium-derived hyperpolarizing factor: a modulator of arterial compliance. Circ Res 82:696–703

Anmerkungen

Die Quelle ist am Ende genannt, der Umfang der Übernahme (die auf der Vorseite beginnt), ist aber so nicht gekennzeichnet, auch weil es zahlreiche andere Literaturverweise gibt.

Sichter
(Hindemith) Klgn

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