Pump perfusion causes vasodilation by activation of platelets

Use of a pump in extracorporeal circuits depresses autoregulation and vascu lar tone. To study whether platelets are involved, we perfused rat hindlegs by means of an extracorporeal shunt between carotid and femoral artery. Au toperfusion could instantaneously be replaced by pump perfusion. To avoid i nterference by effects caused by blood-material contact, the circuit was co ated with albumin. Spontaneous flow did not elicit platelet aggregation as recorded continuously with a photometric device inserted into the tubing, n or did it affect femoral vascular resistance. However, pump perfusion immed iately evoked strong platelet aggregation that stabilized at a lower level after 2-3 minutes. Femoral resistance rose slightly during the first 2 minu tes, but thereafter fell to 63% of control and stayed at approximately 70% for the next 2 hours. Pump induced platelet aggregation and fall in vascula r resistance could be prevented with aurintricarboxylic acid, which specifi cally inhibits shear induced platelet aggregation. We conclude that pump pe rfusion with blood in coated systems elicits shear-induced platelet aggrega tion that, in turn, leads to vasodilation in the perfused vascular bed. The se effects can be prevented by blocking the binding of von Willebrand facto r to the platelet glycoprotein Ib receptors.