CONTEXT: Studies of platelet function in diabetics are inconsistent, some studies reporting higher platelet reactivity, while others showed no change. OBJECTIVE: We aimed to evaluate platelet indices and in vitro platelet aggregation in rats with long-lasting (28 weeks) diabetes mellitus. DESIGN: Twelve controls and 14 diabetic rats were investigated. Diabetes was induced in 11-week-old rats using streptozotocin (60 mg/kg,i.p.). Platelet indices and in vitro adenosine diphosphate (ADP)-, protease-activated receptor 4 (PAR4) agonist-, and arachidonic acid (AA)-induced platelet aggregation were assessed at the age of 38 weeks. RESULTS: Compared to controls, diabetic rats presented lower platelet count and plateletcrit (both p≤0.001), and higher mean platelet volume (p<0.01). ADP- (p=0.04) and AA-induced (p<0.01) platelet aggregation were lower in diabetic compared with control rats, whereas PAR4 agonist-induced platelet aggregation was similar between the two groups (p=1.00). CONCLUSIONS: This study demonstrates a paradox of high intrinsic platelet reactivity and low in vitro ADP- and AA-induced platelet aggregation in diabetic rats compared with non-diabetic controls. The relevance of in vitro platelet aggregation to the contribution of platelets to in vivo thromboembolic events in diabetic rats remains questionable.
CONTEXT: Studies of platelet function in diabetics are inconsistent, some studies reporting higher platelet reactivity, while others showed no change. OBJECTIVE: We aimed to evaluate platelet indices and in vitro platelet aggregation in rats with long-lasting (28 weeks) diabetes mellitus. DESIGN: Twelve controls and 14 diabetic rats were investigated. Diabetes was induced in 11-week-old rats using streptozotocin (60 mg/kg,i.p.). Platelet indices and in vitro adenosine diphosphate (ADP)-, protease-activated receptor 4 (PAR4) agonist-, and arachidonic acid (AA)-induced platelet aggregation were assessed at the age of 38 weeks. RESULTS: Compared to controls, diabetic rats presented lower platelet count and plateletcrit (both p≤0.001), and higher mean platelet volume (p<0.01). ADP- (p=0.04) and AA-induced (p<0.01) platelet aggregation were lower in diabetic compared with control rats, whereas PAR4 agonist-induced platelet aggregation was similar between the two groups (p=1.00). CONCLUSIONS: This study demonstrates a paradox of high intrinsic platelet reactivity and low in vitro ADP- and AA-induced platelet aggregation in diabetic rats compared with non-diabetic controls. The relevance of in vitro platelet aggregation to the contribution of platelets to in vivo thromboembolic events in diabetic rats remains questionable.
Authors: Robert J Huggett; Eleanor M Scott; Stephen G Gilbey; John B Stoker; Alan F Mackintosh; David A S G Mary Journal: Circulation Date: 2003-12-15 Impact factor: 29.690
Authors: Paolo Gresele; Giuseppe Guglielmini; Massimiliano De Angelis; Silvia Ciferri; Marco Ciofetta; Emanuela Falcinelli; Carlo Lalli; Giovanni Ciabattoni; Giovanni Davì; Geremia B Bolli Journal: J Am Coll Cardiol Date: 2003-03-19 Impact factor: 24.094