Pump perfusion causes vasodilation by activation of platelets

Area of Science:

• Physiology
• Biomedical Engineering
• Hematology

Background:

• Extracorporeal circuits often employ pumps, which can alter physiological autoregulation and vascular tone.
• The precise mechanisms by which pump use affects vascular function, particularly the role of platelets, remain incompletely understood.

Purpose of the Study:

• To investigate the involvement of platelets in the depression of autoregulation and vascular tone observed during pump perfusion in extracorporeal circuits.
• To elucidate the relationship between pump-induced shear stress, platelet aggregation, and subsequent changes in vascular resistance.

Main Methods:

• Rat hindlegs were perfused using an extracorporeal shunt, allowing seamless transition between autoperfusion and pump perfusion.
• Albumin coating of the circuit minimized blood-material interactions.
• Platelet aggregation was monitored photometrically, and femoral vascular resistance was measured.
• Aurintricarboxylic acid was used to inhibit shear-induced platelet aggregation.

Main Results:

• Pump perfusion, unlike autoperfusion, induced significant platelet aggregation.
• Pump perfusion led to a decrease in femoral vascular resistance, indicating vasodilation.
• The administration of aurintricarboxylic acid prevented both pump-induced platelet aggregation and the subsequent vasodilation.

Conclusions:

• Pump perfusion in extracorporeal circuits elicits shear-induced platelet aggregation.
• This platelet aggregation is a key mediator of the observed vasodilation and reduced vascular tone.
• Targeting the interaction between von Willebrand factor and platelet glycoprotein Ib receptors can prevent these pump-induced effects.