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Acta Physiologica Congress

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Acta Physiologica 2006; Volume 186, Supplement 650
Joint Meeting of The German Society of Physiology and The Federation of European Physiological Societies 2006
3/26/2006-3/29/2006
Ludwig-Maximilians-University, Munich


REMODELING OF BLOOD VESSELS
Abstract number: OW01-5

Pries1 AR, Reglin1 B, Zakrzewicz1 A, Secomb1 TW

1Physiologisches Institut, Charite - CBF, Berlin

Continuous structural adaptation of small blood vessels is crucial for long-term control of tissue perfusion and peripheral resistance. It has significant importance for conditions like hypertension or collateralization. Here, a model is presented which explains experimentally observed distributions of vessel diameter and wall thickness in microvascular networks by a generic set of structural responses by vessel segments to local stimuli. Diameter and wall mass of each segment were assumed to vary in response to fluid shear stress, circumferential wall stress, and tissue metabolic status, as indicated by local partial pressure of oxygen. Metabolic signals were assumed to be propagated upstream and downstream along vascular segments. The following features were found to be essential: increased wall shear stress and increased metabolic signal stimulate increases in diameter; increased circumferential stress stimulates increase in wall mass; the wall stress derived stimulus decreases with increasing wall thickness. Predicted relationships in vascular networks between pressure and shear stress, and between diameter and circumferential stress, were then consistent with experimental observations. In addition, peripheral resistance increases by about 65% for an increase in driving pressure from 50 to 150 mmHg. This approach allows analysis and prediction of structural vascular responses and their functional implications under normal and pathophysiological conditions, as for example during development of hypertension.

To cite this abstract, please use the following information:
Acta Physiologica 2006; Volume 186, Supplement 650 :OW01-5

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