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J Thorac Cardiovasc Surg 2006;131:813-821
© 2006 The American Association for Thoracic Surgery

Cardiopulmonary Support and Physiology

Pump-induced platelet aggregation with subsequent hypotension: Its mechanism and prevention with clopidogrel

Institute for Cardiovascular Research, Vrije Universiteit Medical Center, Amsterdam, The Netherlands

Received for publication August 16, 2005; revisions received October 10, 2005; accepted for publication October 11, 2005.

^_* Address for reprints: P. Borgdorff, PhD, Laboratory for Physiology, VUMC, Van der Boechorststraat 7, 1081 BT Amsterdam, The Netherlands. (Email: p.borgdorff{at}vumc.nl).

OBJECTIVES: Use of extracorporeal circuits in cardiopulmonary bypass and hemodialysis often causes bleeding problems and hypotension. As shown previously, this might be caused by activation of blood platelets due to pumping. The present study investigates the mechanism of pump-induced platelet aggregation and its possible prevention.

METHODS AND RESULTS: Continuous measurement of platelet aggregation in an extracorporeal shunt from a carotid to a femoral artery in rats showed that aggregation during the first 10 minutes of pumping was not reduced by coating the tube with albumin or heparin nor by using dalteparin instead of unfractionated heparin as anticoagulant. Also, pump characteristics seemed unimportant because aggregation could already be elicited by single tube compression with one pump roller. It was calculated that during compression wall shear stress in the tube rises far beyond the values known to induce platelet aggregation, occurring also in clinically used roller pumps. A crucial role for adenosine diphosphate was demonstrated by blockade of platelet adenosine diphosphate-P2Y₁₂ receptors with the clinically used drug clopidogrel (50 mg/kg intravenously, n = 8). This prevented platelet aggregation and the fall of systemic blood pressure (to 71% ± 12% in controls, n = 6) during 2 hours of continuous pumping.

CONCLUSION: We conclude that pump-induced platelet aggregation is not caused by factors released from the tube or its coating but is initiated by short bouts of high shear stress, and its continuation is critically dependent on adenosine diphosphate. The latter might have clinical relevance for patients connected to extracorporeal systems.

This article has been cited by other articles:

				P. Borgdorff, G. J. Tangelder, and W. J. Paulus Cyclooxygenase-2 Inhibitors Enhance Shear Stress-Induced Platelet Aggregation J. Am. Coll. Cardiol., August 15, 2006; 48(4): 817 - 823. [Abstract] [Full Text] [PDF]