Editorials |
From the Cardiovascular Research Center Inserm Lariboisière, Inserm U689, University Paris 7
Correspondence to Bernard Lévy, Inserm U689, Cardiovascular Research Center Inserm Lariboisière, 41 Bd de la Chapelle, 75010 Paris, France. E-mail levy@larib.inserm.fr
See related article, pages 656662
Key Words: collateral arteries shear stress ischemia
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
The primary role of the vascular system is to carry blood and oxygen to tissue. This task is complicated by the vastly differing needs of tissues for oxygen according to their metabolism. Moreover, the metabolic activity in a given organ, and thereby its need of blood flow and oxygen, may dramatically change in time scales varying from seconds (during the onset of muscular exercise for example) to months or years (growth of organs, ischemic processes). Therefore, to ensure good organ function, the vasculature must adapt to these heterogeneous needs. Because blood vessels are highly distributed in space, one marvels at how a vascular bed manages to adapt structurally to the local environment, and how individual segments within the vascular network succeed in supplying the right amount of blood and oxygen to tissues in the most economical way. In fact, such intricate control requires 2 adaptation processes that exist in parallel: short term release of vasoactive agonists or changes in vascular tone provide a quick functional adaptation to accommodate rapid changes in metabolic demand, whereas growth or regression of blood vessels (termed vascular remodeling) represent long term structural adaptation to new, lasting metabolic and blood flow conditions (Figure 1). Both acute and chronic adaptations are complementary and are driven by the same environmental variables, which include local oxygen tension, vascular wall tension, and shear stress. For example, when arteries remodel in response to a new and lasting elevated blood flow, the initial acute vasodilation, mediated by endothelium-derived nitric oxide
Related Article:
Circ. Res. 2006 99: 656-662.
|
Circulation Research Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 2006 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |