Background: Despite meticulous investigation of bypass techniques for DHCA, unfavorable long-term neurologic deficits have been well documented. Our aim was to improve brain perfusion by reducing platelet plugging using a GPIIb/IIIa-Inhibitor (Eptifibatide) in an experimental model of DHCA / reperfusion in pigs.
Methods: Two groups of 12 piglets each (Eptifibatide versus control) underwent 10-minute normothermic bypass, 40-minute cooling on cardiopulmonary bypass [CPB] (Hct 30%, CPB-flow 100ml/kg/min), 60-minute circulatory arrest at 15 °C, and 40-minute rewarming. Intravital fluorescence microscopy of pial vessels, immunohistological and electron microscopic studies were performed.
Results: In the control group an increase in platelet adhesion and a decrease in microvascular perfusion were measured, the functional capillary density [FCD] being 72±4% compared to baseline at 10 minutes of reperfusion. Perivascular cerebral alterations were documented. At the same time point of reperfusion, the Eptifibatide group demonstrated a decreased platelet adhesion and aggregation (- 70% compared to the control group), the FCD being preserved (96±3% relative to baseline). A more rapid recovery of tissue oxygenation (recovery time to reach baseline values was 5 minutes versus 30 minutes, p = 0.02) was documented. The use of Eptifibatide resulted in less ultrastructural cerebral changes and a reduced activation of brain cell apoptosis (p = 0.05).
Conclusions: Platelet plugging reduction by use of GPIIb/IIIa-Inhibitor provides adequate cerebral capillary blood flow and prevents cerebral ischemia. Furthermore, significant hypoxic endothelial cell injury and perivascular brain tissue damage reduction can be achieved.

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