© 1999 by European Society of Cardiology
Copyright © 1999, European Society of Cardiology
Arteriogenesis, the good and bad of it
Department for Experimental Cardiology, Max-Planck-Institute for Physiological and Clinical Research, Bad Nauheim, Germany
* Corresponding author. Tel.: +49-6032-705-402; fax: +49-6032-705-419 w.schaper@kerckhoff.mpg.de
Received 31 May 1999; accepted 31 May 1999
| The first 10% of the full text of this article appears below. |
Arteriolar vessels that interconnect adjacent vascular territories in the form of networks or arcades exist normally in the skeletal [1] and cardiac muscle [2] of most mammals including man. They function usually as a means of efficient flow distribution, to act as capacitors for blood displacement in non-synchronously contracting muscles or are just remnants of the embryonic vascular network that has not fully reached its full determination.
These vessels can expand by growth when pressure gradients develop, the most likely cause of which is the unilateral fall in pressure by a stenosis or occlusion of one of the arteries that feed into the network [2]. Although total blood flow into the network is now reduced (or unaltered due to compensating vasodilation) the velocity of blood flow in the vessels representing the shortest connection to the distal distribution of the occluded vessel is markedly increased. This creates an increase
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1 The role of tissue ischemia |
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2 Summary |
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