Figure 3
Figure 3. Prothrombin consumption and thrombin formation. (A) Prothrombin activation in bleeding-time blood. A representative immunoblot of prothrombin on a nonreduced gel (5%-15%) from a patient with stable CAD and a patient with AMI. Prothrombin concentrations, determined by quantitative densitometry of immunoblots, are presented as a function of time (seconds) for all patients in each cohort; stable CAD (▵, n = 28), AMI (▴, n = 28), and heparin-treated AMI (■, n = 8). Data are plotted as means plus or minus SEM. (B) A representative reduced immunoblot (5%-15%) for thrombin B-chain formation in bleeding-time blood. Thrombin B-chain concentration is presented as a function of time (seconds) for patients with stable CAD (▵, n = 28), AMI (▴, n = 28), and heparin-treated AMI (■, n = 8). Data are plotted as means plus or minus SEM. Historic data for healthy individuals on aspirin (●, ) are presented for comparison.

Prothrombin consumption and thrombin formation. (A) Prothrombin activation in bleeding-time blood. A representative immunoblot of prothrombin on a nonreduced gel (5%-15%) from a patient with stable CAD and a patient with AMI. Prothrombin concentrations, determined by quantitative densitometry of immunoblots, are presented as a function of time (seconds) for all patients in each cohort; stable CAD (▵, n = 28), AMI (▴, n = 28), and heparin-treated AMI (■, n = 8). Data are plotted as means plus or minus SEM. (B) A representative reduced immunoblot (5%-15%) for thrombin B-chain formation in bleeding-time blood. Thrombin B-chain concentration is presented as a function of time (seconds) for patients with stable CAD (▵, n = 28), AMI (▴, n = 28), and heparin-treated AMI (■, n = 8). Data are plotted as means plus or minus SEM. Historic data for healthy individuals on aspirin (●, ) are presented for comparison.

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