Time course of changes in in vitro platelet function and plasma von willebrand factor activity (VIIIR:WF) and factor VIII-related antigen (VIIIR:Ag) in the diabetic rat.
Time course of changes in in vitro platelet function and plasma von willebrand factor activity (VIIIR:WF) and factor VIII-related antigen (VIIIR:Ag) in the diabetic rat.
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糖尿病大鼠体外血小板功能和血浆血管性血友病因子活性 (VIIIR:WF) 和因子 VIII 相关抗原 (VIIIR:Ag) 变化的时间过程。
DOI：
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发表时间：
1983
期刊：
影响因子：
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通讯作者：
J. Colwell
中科院分区：
文献类型：
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作者：
P. Winocour;M. Lopes;M. Laimins;J. Colwell
糖尿病患者血小板异常与血管壁变化之间的关系尚不清楚。我们检查了链脲佐菌素诱导的糖尿病大鼠体外血小板功能和内皮损伤改变的时间过程，通过测量血管性血友病因子 (VIIIR:WF) 和因子 VIII 相关抗原 (VIIIR:Ag) 的血浆水平进行评估。在诱导糖尿病后3、7、14或28天的大鼠和对照动物中制备洗涤的血小板悬浮液，测量响应ADP、凝血酶和胶原的血小板聚集和血小板释放反应。与对照血小板相比，糖尿病动物的血小板早在糖尿病诱导后 3 天就表现出对 ADP 的聚集反应增强，并在 7 天后变得对凝血酶过度反应。第 14 天时，糖尿病动物的血小板中凝血酶诱导的血清素释放量更大。在任何研究时间，胶原蛋白引起的反应都没有不同。 VIIIR:WF通过凝胶过滤血小板中瑞斯托菌素诱导的血小板凝集时间测定，VIIIR:Ag通过免疫电泳技术测定。诱导糖尿病后 28 天，大鼠血浆中的 VIIIR:WF 和 VIIIR:Ag 显着增强，诱导糖尿病后 14 天，大鼠血浆中的 VIIIR:Ag 显着增强，但在研究的早期时间，两者与对照治疗大鼠血浆中的值没有差异。因此，VIIIR:WF 和 VIIIR:Ag 的变化晚于血小板功能的变化。血浆胆固醇浓度在任何研究时间都没有显着差异，但血浆甘油三酯浓度在第3天显着增加，并且随着糖尿病持续时间的延长而保持增加。这可能导致了观察到的血小板和血管壁的变化。如果这些体外变化反映了体内行为，那么血小板变化发生在血管壁变化之前，因此似乎不是实验性糖尿病中此类变化的结果。
The relationship between platelet abnormalities and vessel wall changes in diabetes is not known. We have examined the time course of alterations in in vitro platelet function and endothelial damage, as assessed by measurement of plasma levels of von Willebrand factor (VIIIR:WF) and factor VIII-related antigen (VIIIR:Ag), in streptozotocin-induced diabetic rats. Platelet aggregation and the platelet release reaction in response to ADP, thrombin, and collagen were measured in suspensions of washed platelets prepared from rats 3, 7, 14, or 28 days after induction of diabetes and in control animals. Platelets from diabetic animals showed enhanced aggregation response to ADP as early as 3 days after induction of diabetes and became hyperresponsive to thrombin after 7 days, compared to control platelets. Thrombin-induced release of serotonin was greater in platelets from diabetic animals at 14 days. Collagen-induced responses were not different at any time studied. VIIIR:WF was determined by ristocetin-induced platelet agglutination time in gel-filtered platelets, and VIIIR:Ag was determined by immunoelectrophoretic technique. VIIIR:WF and VIIIR:Ag were significantly enhanced in plasma from rats at 28 days after induction of diabetes and VIIIR:Ag was enhanced in plasma from rats at 14 days after induction of diabetes, but at the earlier times studied, neither were different from values in plasma from control-treated rats. Changes in VIIIR:WF and VIIIR:Ag therefore occurred later than the changes in platelet function. Plasma cholesterol concentrations were not significantly different at any of the times studied, but plasma triglyceride concentrations were significantly increased at 3 days and remained increased with further durations of diabetes. This may have contributed to the observed platelet and vessel wall changes. If these in vitro alterations reflect in vivo behavior, then platelet alterations occur before vessel wall changes and therefore do not appear to be a consequence of such changes in experimental diabetes mellitus.