PLATELET AND FIBRIN NETWORK MORPHOL- OGY ALTERATIONS IN A RABBIT MODEL OF DIET IN-DUCED CARDIOMETABOLIC SYNDROME

MEDINA, MIRTA; ALARCÓN, GABRIELA; ROCO, JULIETA; MEDINA, ANALIA; ERINBAGUE, MARTA

Congreso; Reunión Conjunta de Sociedades de Biociencias; 2017

The cardiometabolic syndrome (CMS) is a constellation of inter-related risk factors of metabolic origins that together promote theincreased risk of cardiovascular disease (CVD). Central obesitywith the associated CMS components promotes proinflammatoryand prothrombotic states. The aim of the present work was studywhether platelet and fibrin network-morphology or coagulation pro-files was altered in a rabbit model of CMS. Male rabbits were fedeither a control diet (CD) or atherogenic high fat diet (18 % fat and1 % cholesterol, HFD-HC) during 6 weeks. Scanning electron mi-croscopy was used to study platelet- and fibrin network-morphologyby preparing platelet-rich plasma (PRP). Ten μl of PRP was usedto study platelet morphology and 10 μl of PRP was mixed with 5 μlof bovine thrombin (2,7UI/ml) to study fibrin network morphology.Activated Partial Thromboplastin Time (APTT), thombin time andplatelets count were performed. Platelets of the CD appeared spher-ical with few pseudopodia present while the platelets of the CMSpresented with numerous pseudopodia and spreading, indicatingactivation. The fibrin networks of the CD consist of thick and thinfibers that form an organized network of fibers. The fibrin networksof the CMS appeared less organized with less taut fibers. Fibrin fiberthickness was found to be significantly increased in the CMS group(p-value 0.05) fromthe CD, indicating a normal functioning coagulation cascade. Thefindings indicate that premature activation of platelets (as a resultof chronic inflammation) that in turn causes altered fibrin formationbut not alterations in the coagulation cascade may account for theprothrombotic status in the CMS.