[Is the tonisation of varicose veins due to elevated prostacyclin synthesis caused by dihydroergotamine?].
Prostacyclin is the most potent inhibitor of platelet aggregation and a very strong vasodilator. A few reports on a moderate vasoconstrictory response in certain vascular segments in various species have received less attention. We demonstrated recently that PGI2 dilates the arterial wall and has a constrictory effect on the venous wall. Normal and varicose human veins show a dose-dependent constrictory response to PGI2. Pretreatment of patients with 2.5 mg dihydroergotamine t.i.d. for 10 days increases venous PGI2 synthesis significantly. In vitro contractility response is identical in normal and varicose veins. Furthermore, no difference in contractility was registered in veins derived from treated and untreated patients. The significantly enhanced formation of PGI2 evoked by dihydroergotamine might be responsible for the tonisation of normal, healthy veins, as well as varicose veins.
D000328:Adult; D004087:Dihydroergotamine / Q000627:therapeutic use*; D011464:Epoprostenol / Q000096:biosynthesis*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D014648:Varicose Veins / Q000188:drug therapy*; D014661:Vasoconstriction / Q000187:drug effects
D004087:Dihydroergotamine; D011464:Epoprostenol
Werden varikös veränderte Venen durch Dihydroergotamin über eine gesteigerte Prostacyclinsynthese tonisiert?