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Platelet activation supports the development of venous thrombosis in hyperlipidemic rats

 

作者: A. Cignarella,   L. Mussoni,   L. Mannucci,   E. Ferioli,   L. Puglisi,   E. Tremoli,  

 

期刊: Blood Coagulation and Fibrinolysis  (OVID Available online 1998)
卷期: Volume 9, issue 1  

页码: 47-54

 

ISSN:0957-5235

 

年代: 1998

 

出版商: OVID

 

关键词: venous thrombosis;hyperlipidemia;Yoshida rats;streptozotocin;diabetes;thromboxane

 

数据来源: OVID

 

摘要:

This investigation sought to determine how different components of the hemostatic system affect the development of venous thrombosis in rats displaying hyperlipidemia, either on a genetic basis or secondary to metabolic disorders. On employing an experimental model of collagen-triggered venous thrombosis, both spontaneously hyperlipidemic (Yoshida strain) and streptozoto-cin-induced diabetic rats generated about 2.3-fold greater thrombi than normolipidemic controls. This was associated with significant platelet activation, as revealed by increased levels of serum thromboxane B2in diabetics (1.5-fold) as well as in Yoshida (8-fold) rats, in comparison with controls. In contrast, ex vivo total fibrinolytic activity, as measured by euglobulin lysis time, did not differ between normo- and hyperlipidemic or diabetic animals. Plasminogen activator inhibitor activity was lower in both Yoshida and diabetic rats than in controls. However, tissue-type plasminogen activator activity was differently affected by the genetic or the diabetes-related hyperlipidemia, showing significantly lower values in Yoshida (-26%), but significantly higher values in diabetic rats (+29%) than in normolipidemic controls. We conclude that platelet activation, rather than consistent modifications of the fibrinolytic system, is likely to influence the enhanced thrombus development associated with primary or secondary forms of hyperlipidemia. Blood Coag Fibrinol 9:47–53 × 1998 Rapid Science Ltd.

 

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