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Am J Physiol Regul Integr Comp Physiol (July 25, 2002). doi:10.1152/ajpregu.00006.2002
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Articles in PresS, published online ahead of print July 25, 2002
Am J Physiol Regu Physiol, 10.1152/ajpregu.00006.2002
Submitted on January 7, 2002
Accepted on July 15, 2002

"Sausage-string" appearance of arteries and arterioles can be caused by an instability of the blood vessel wall

Jens Christian B Jacobsen1, Ulrik Beierholm2, Rene Mikkelsen2, Finn Gustafsson1, Preben Alstrom2, and Niels-Henrik Holstein-Rathlou1*

1 Department of Medical Physiology, The University of Copenhagen, Copenhagen, Denmark
2 The Niels Bohr Institute, The University of Copenhagen, Copenhagen, Denmark

* To whom correspondence should be addressed. E-mail: nhhr{at}mfi.ku.dk.

Vascular damage induced by acute hypertension is preceded by a peculiar pattern where blood vessels show alternating regions of constrictions and dilations ("sausages-on-a-string"). The pattern occurs in the smaller blood vessels, and it plays a central role in causing the vascular damage. A related vascular pattern has been observed in larger vessels from several organs during angiography. In the larger vessels the occurrence of the pattern does not appear to be related to acute hypertension. A unifying feature between the phenomenon in large and small vessels seems to be an increase in vascular wall tension. Despite much research, the mechanisms underlying the "sausage" pattern have remained unknown. Here we present an anisotropic model of the vessel wall, and show that the "sausage" pattern can arise due to an instability of the vessel wall. The model reproduces many of the key features observed experimentally. Most importantly, it suggests that the "sausaging" phenomenon is neither caused by a mechanical failure of the vessel wall due to a high blood pressure, nor is it due to standing pressure waves caused by the beating of the heart. Rather, it is the expression of a general instability phenomenon. Experimental data suggest that the structural changes induced by the instability may cause secondary damage to the wall of small arteries and arterioles in the form of endothelial hyperpermeability followed by local fibrinoid necrosis of the vascular wall.







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