OBJECTIVE: To compare platelet plasminogen activator inhibitor 1 (PAI-1) release in type II diabetic patients and healthy control subjects. RESEARCH DESIGN AND METHODS: We studied a group of 27 diabetic patients and a group of 16 nondiabetic control subjects. Whole-blood platelet aggregation, defined as a decrease in platelet count during shaking (180 rpm) of blood samples at 37 degrees C, and plasma PAI-1 antigen concentrations were measured in parallel at time 0, 7.5, 15, 30, 60, 120, and 180 min. RESULTS: Platelet aggregation did not differ significantly between the two groups at any time period. However, the increase in plasma PAI-1 antigen concentration over basal levels at time 0 was higher for the group of diabetic patients when compared with their matched control subjects. The increment of PAI-1 antigen was 61.8 +/- 29.4 vs. 35.9 +/- 13.4 ng/ml (P < 0.005, means +/- SD) after 180 min for the diabetic and control subjects, respectively. Platelet PAI-1 release was correlated to very-low-density lipoprotein cholesterol and triglyceride plasma levels, but not to HbA1c levels. CONCLUSIONS: Platelets of patients with type II diabetes release significantly more PAI-1 than platelets of healthy subjects at the same level of platelet aggregation. This may contribute to enhanced thrombosis in diabetes.
OBJECTIVE: To compare platelet plasminogen activator inhibitor 1 (PAI-1) release in type II diabeticpatients and healthy control subjects. RESEARCH DESIGN AND METHODS: We studied a group of 27 diabeticpatients and a group of 16 nondiabetic control subjects. Whole-blood platelet aggregation, defined as a decrease in platelet count during shaking (180 rpm) of blood samples at 37 degrees C, and plasma PAI-1 antigen concentrations were measured in parallel at time 0, 7.5, 15, 30, 60, 120, and 180 min. RESULTS:Platelet aggregation did not differ significantly between the two groups at any time period. However, the increase in plasma PAI-1 antigen concentration over basal levels at time 0 was higher for the group of diabeticpatients when compared with their matched control subjects. The increment of PAI-1 antigen was 61.8 +/- 29.4 vs. 35.9 +/- 13.4 ng/ml (P < 0.005, means +/- SD) after 180 min for the diabetic and control subjects, respectively. Platelet PAI-1 release was correlated to very-low-density lipoprotein cholesterol and triglyceride plasma levels, but not to HbA1c levels. CONCLUSIONS: Platelets of patients with type II diabetes release significantly more PAI-1 than platelets of healthy subjects at the same level of platelet aggregation. This may contribute to enhanced thrombosis in diabetes.