Figure 5.
Figure 5. Kinetics of platelet accumulation during thrombus formation following laser-induced endothelial cell injury in the presence of cilostazol or JF959602. (A) In the presence of 10 mg/kg cilostazol (n = 28), a statistically significant decrease in the median of maximum platelet accumulation compared with the saline vehicle control (P < .05, n = 32) was observed. Inhibition of maximum platelet accumulation by 10 mg/kg cilostazol was similar to that observed using 1.2 mg/kg JF959602. (B) Similar to 1.2 mg/kg JF959602, 10 mg/kg cilostazol significantly inhibited (P < .05, n = 28) the median stabilized platelet accumulation in comparison to the saline vehicle control (n = 36). (C) Inhibition of PDE3A activity by the infusion of either 1.2 mg/kg JF959602 (n = 30, gray lines) or 10 mg/kg cilostazol (n = 29, black lines) resulted in inhibition of platelet accumulation in a similar pattern. (D) Rate of platelet accumulation into thrombi over time in the presence of JF959602 or cilostazol was obtained by plotting the derivative of the kinetic curve illustrated in panel C. Both PDE3A inhibitors were found to decrease the maximal rate of platelet accumulation without affecting the time for thrombosis to reach the maximum rate and the time to maximal platelet accumulation, as indicated by the point at which the rate of platelet accumulation intersects the ordinate.

Kinetics of platelet accumulation during thrombus formation following laser-induced endothelial cell injury in the presence of cilostazol or JF959602. (A) In the presence of 10 mg/kg cilostazol (n = 28), a statistically significant decrease in the median of maximum platelet accumulation compared with the saline vehicle control (P < .05, n = 32) was observed. Inhibition of maximum platelet accumulation by 10 mg/kg cilostazol was similar to that observed using 1.2 mg/kg JF959602. (B) Similar to 1.2 mg/kg JF959602, 10 mg/kg cilostazol significantly inhibited (P < .05, n = 28) the median stabilized platelet accumulation in comparison to the saline vehicle control (n = 36). (C) Inhibition of PDE3A activity by the infusion of either 1.2 mg/kg JF959602 (n = 30, gray lines) or 10 mg/kg cilostazol (n = 29, black lines) resulted in inhibition of platelet accumulation in a similar pattern. (D) Rate of platelet accumulation into thrombi over time in the presence of JF959602 or cilostazol was obtained by plotting the derivative of the kinetic curve illustrated in panel C. Both PDE3A inhibitors were found to decrease the maximal rate of platelet accumulation without affecting the time for thrombosis to reach the maximum rate and the time to maximal platelet accumulation, as indicated by the point at which the rate of platelet accumulation intersects the ordinate.

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