{"title":"Refractoriness of diabetic platelets to inhibitory prostaglandins","authors":"M. Lagarde, P. Berciaud, M. Burtin, M. Dechavanne","doi":"10.1016/0161-4630(81)90138-5","DOIUrl":null,"url":null,"abstract":"<div><p>Inhibition of collagen-induced platelet aggregation by either endothelial extracts, prostacyclin, prostaglandin E<sub>1</sub> or prostaglandin D2 was investigated. The inhibition was less efficient with diabetic platelets than with platelets from normal donors. The refractoriness of diabetic platelets to inhibitory prostaglandins was observed both with platelet-rich plasma and platelets isolated from their plasma. Moreover, levels of cyclic AMP in resting platelets and after stimulation by either PGE<sub>1</sub> or PGD<sub>2</sub> were lower in diabetic platelets than in normal platelets. It is concluded that the weaker response of diabetic platelets to inhibitory prostaglandins could be related to their content in cyclic AMP.</p></div>","PeriodicalId":76381,"journal":{"name":"Prostaglandins and medicine","volume":"7 4","pages":"Pages 341-347"},"PeriodicalIF":0.0000,"publicationDate":"1981-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0161-4630(81)90138-5","citationCount":"21","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Prostaglandins and medicine","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/0161463081901385","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 21
Abstract
Inhibition of collagen-induced platelet aggregation by either endothelial extracts, prostacyclin, prostaglandin E1 or prostaglandin D2 was investigated. The inhibition was less efficient with diabetic platelets than with platelets from normal donors. The refractoriness of diabetic platelets to inhibitory prostaglandins was observed both with platelet-rich plasma and platelets isolated from their plasma. Moreover, levels of cyclic AMP in resting platelets and after stimulation by either PGE1 or PGD2 were lower in diabetic platelets than in normal platelets. It is concluded that the weaker response of diabetic platelets to inhibitory prostaglandins could be related to their content in cyclic AMP.