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Effects of desmopressin on thrombogenesis in aspirin‐induced platelet dysfunction
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Summary. Aspirin causes a coagulation disorder. Desmopressin has haemostatic effects by increasing the plasma levels of coagulation factor VIII and von Willebrand factor. The precise effects of desmopressin on thrombogenesis are not known. In an in vivo model, we investigated the effect of the drug on thrombus formation and platelet function after aspirin use. Male Lewis rats weighing 250–300 g were used. Four groups with 10 animals each were formed: control, aspirin, desmopressin and aspirin + desmopressin. In each animal, the femoral artery was dissected. A thrombogenic vessel injury was created by inverting a full thickness portion of the proximal edge of the incised artery into the lumen. The following parameters were measured: maximum thrombus size, time period until maximum thrombus size was reached and overall platelet function. In addition, the thrombi generated were investigated histologically. Thrombus formation time was significantly shorter with desmopressin compared with the animals treated with aspirin (P < 0·0001) and controls (P = 0·008). Maximum thrombus size was larger in the desmopressin and desmopressin + aspirin groups when compared with the group treated with aspirin only. Overall platelet function was significantly enhanced with desmopressin compared with controls (P = 0·025) and with aspirin (P < 0·0001). The differences were confirmed histologically. In conclusion, desmopressin significantly accelerates thrombus formation in aspirin‐treated animals. It can also re‐establish thrombus size after the use of aspirin. Overall platelet function is significantly increased by desmopressin.
Title: Effects of desmopressin on thrombogenesis in aspirin‐induced platelet dysfunction
Description:
Summary.
Aspirin causes a coagulation disorder.
Desmopressin has haemostatic effects by increasing the plasma levels of coagulation factor VIII and von Willebrand factor.
The precise effects of desmopressin on thrombogenesis are not known.
In an in vivo model, we investigated the effect of the drug on thrombus formation and platelet function after aspirin use.
Male Lewis rats weighing 250–300 g were used.
Four groups with 10 animals each were formed: control, aspirin, desmopressin and aspirin + desmopressin.
In each animal, the femoral artery was dissected.
A thrombogenic vessel injury was created by inverting a full thickness portion of the proximal edge of the incised artery into the lumen.
The following parameters were measured: maximum thrombus size, time period until maximum thrombus size was reached and overall platelet function.
In addition, the thrombi generated were investigated histologically.
Thrombus formation time was significantly shorter with desmopressin compared with the animals treated with aspirin (P < 0·0001) and controls (P = 0·008).
Maximum thrombus size was larger in the desmopressin and desmopressin + aspirin groups when compared with the group treated with aspirin only.
Overall platelet function was significantly enhanced with desmopressin compared with controls (P = 0·025) and with aspirin (P < 0·0001).
The differences were confirmed histologically.
In conclusion, desmopressin significantly accelerates thrombus formation in aspirin‐treated animals.
It can also re‐establish thrombus size after the use of aspirin.
Overall platelet function is significantly increased by desmopressin.
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