Glycoprotein IIb/IIIa receptor inhibitor attenuates platelet aggregation induced by thromboxane A2 during in vitro nonpulsatile ventricular assist circulation

A recent development in antithrombotic research allows the inhibition of platelet aggregation via protection of the glycoprotein IIb/IIIa receptor on the platelet membrane. We hypothesized that a GP IIb/IIIa receptor inhibitor would inhibit thromboxane-induced platelet aggregation during circulation in our in vitro ventricular assist device (VAD) circuit and preserve long-term platelet function. Twenty-one in vitro nonpulsatile centrifugal VAD circuits were simulated for 4 days using 450 ml of fresh human whole blood with or without glycoprotein IIb/IIIa receptor inhibitor (tirofiban). Platelet aggregation and degranulation were measured in whole blood induced by ristocetin, collagen, ADP, and thromboxane A2 (TXA2). The tirofiban-treated group preserved the platelet count and tended to exert these beneficial effects by inhibiting pathologic platelet aggregation induced by TXA2, collagen, and ADP as well as degranulation. Tirofiban may be useful in preserving platelet number and function during clinical VAD use.     

The meaning of the turning point of the index of motor current amplitude curve in controlling a continuous flow pump or evaluation of left ventricular function

In this series, we investigated the meaning of the t-point of index of motor current amplitude (ICA) curve from a point of view of flow rate on in vitro and in vivo studies. On mock circulation loop and left ventricular assist device (LVAD)-equipped pigs, we detected the t-point and compared the pump flow at the t-point with the simultaneous cardiac output. The pump flow at the t-point showed high correlation against the simultaneous cardiac output for in vitro or in vivo study. By detection of the t-point of the ICA curve and measuring or estimating the pump flow at t-point, the cardiac output may be assessed without any sensor in various cardiac conditions.