AJP - Heart Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Heart Circ Physiol 266: H891-H897, 1994;
0363-6135/94 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Borgdorff, P.
Right arrow Articles by van den Bos, G. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Borgdorff, P.
Right arrow Articles by van den Bos, G. C.

AJP - Heart and Circulatory Physiology, Vol 266, Issue 3 891-H897, Copyright © 1994 by American Physiological Society

ARTICLES

Vasodilation by shear-induced platelet aggregation in extracorporeal circuits

P. Borgdorff, W. E. Kok, M. A. Vis and G. C. van den Bos
Laboratory for Physiology, Free University, Amsterdam, The Netherlands.

Extracorporeal circulation may have adverse effects on vascular reactivity. To reduce such effects, we recently coated a tube connecting the carotid and the distal femoral artery of rats with albumin. When we partially occluded this perfusion line, the reduction of flow was followed by a marked increase, which seemed not to be caused by autoregulation but by release of a vasodilator at the site of occlusion. In the present study, we investigated whether this vasodilator could originate from platelets aggregating under the influence of increased shear stress at the site of occlusion. Blood distal to the site of occlusion indeed contained numerous platelet aggregates that were not present before occlusion. Continuous recording with a photometric device showed that aggregation in the tube started before flow increased and ended before flow decreased again. Blockade of serotonin S1- and S2-receptors with methiothepin prevented the flow response. Estimated shear stress (231 +/- 17 dyn/cm2) and shear rate (6,370 +/- 478 s-1) at the site of occlusion were of the magnitude known to elicit platelet aggregation. Others have recently demonstrated that shear-induced platelet aggregation is mediated by binding of von Willebrand factor to platelet glycoprotein Ib, which is inhibited by aurintricarboxylic acid. This drug (35 mg/kg iv) completely abolished both platelet aggregation and flow increase in our experiments. These results suggest that the vasodilation during partial tube occlusion is mediated by serotonin released from platelets that aggregate as a result of high shear stress.


This article has been cited by other articles:


Home page
 J. Thorac. Cardiovasc. Surg.Home page
P. Borgdorff, G. van den Bos, and G. J. Tangelder
Extracorporeal circulation can induce hypotension by both blood-material contact and pump-induced platelet aggregation
J. Thorac. Cardiovasc. Surg., July 1, 2000; 120(1): 12 - 19.
[Abstract] [Full Text] [PDF]

Home page
 J. Thorac. Cardiovasc. Surg.Home page
P. Borgdorff, R. H. van den Berg, M. A. Vis, G. C. van den Bos, and G. J. Tangelder
PUMP-INDUCED PLATELET AGGREGATION IN ALBUMIN-COATED EXTRACORPOREAL SYSTEMS
J. Thorac. Cardiovasc. Surg., November 1, 1999; 118(5): 946 - 952.
[Abstract] [Full Text] [PDF]

Home page
 CirculationHome page
H. Gilutz
Extracorporeal Circulation
Circulation, January 13, 1998; 97(1): 117 - 117.
[Full Text]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online