DECREASED CAPACITY TO INHIBIT PLATELET HYPERACTIVITY AND TO STABILIZEPROSTACYCLIN OF HIGH-DENSITY-LIPOPROTEINS IN EXPERIMENTAL DIABETES

Twenty-eight male Sprague Dawley rats were divided into two groups: a control group (C) of 15 animals and a streptozotocin-induced diabetes group mildly balanced by insulin (D) of 13 animals. After 15 weeks, pl asma and high-density lipoprotein (HDL) lipids were determined in each group. Apoprotein A-I concentration was evaluated in HDL fractions. T he capacity of the HDL fraction to inhibit thrombin and ADP-induced ag gregation of normal platelets was determined for each rat, and in an a dditional experiment the relation dose-effect of HDL was established. The effect of HDL of the two groups on the stabilization of prostacycl in was compared by aggregation bioassay. After 15 weeks, HDL cholester ol (free+esterified) tended to increase in group D compared with group C (P<0.08). By contrast, apoprotein A-I was very significantly decrea sed in HDL-D compared with HDL-C (P<0.001). These alterations were acc ompanied by a significantly decreased capacity of HDL (60 mu g/ml plat elet suspension) to inhibit ADP-induced aggregation (P<0.0001) in grou p D compared with group C. Furthermore, HDL-D incubated 45 or 90 min w ith prostacyclin showed a significantly decreased capacity to stabiliz e prostacyclin compared with HDL-C (P<0.04; P<0.03, respectively). The se alterations in HDL could be involved in thrombosis and atheromatous complications associated with this disease.