Pump perfusion causes vasodilation by activation of platelets.

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Use of a pump in extracorporeal circuits depresses autoregulation and vascular tone. To study whether platelets are involved, we perfused rat hindlegs by means of an extracorporeal shunt between carotid and femoral artery. Autoperfusion could instantaneously be replaced by pump perfusion. To avoid interference by effects caused by blood-material contact, the circuit was coated with albumin. Spontaneous flow did not elicit platelet aggregation as recorded continuously with a photometric device inserted into the tubing, nor did it affect femoral vascular resistance. However, pump perfusion immediately evoked strong platelet aggregation that stabilized at a lower level after 2-3 minutes. Femoral resistance rose slightly during the first 2 minutes, but thereafter fell to 63% of control and stayed at approximately 70% for the next 2 hours. Pump induced platelet aggregation and fall in vascular resistance could be prevented with aurintricarboxylic acid, which specifically inhibits shear induced platelet aggregation. We conclude that pump perfusion with blood in coated systems elicits shear-induced platelet aggregation that, in turn, leads to vasodilation in the perfused vascular bed. These effects can be prevented by blocking the binding of von Willebrand factor to the platelet glycoprotein Ib receptors.