Judge S, Mammen E, Dunbar J C
Department of Physiology, Wayne State University School of Medicine, Detroit, Michigan 48201, USA.
J Assoc Acad Minor Phys. 1995;6(3):100-4.
Previous studies from our laboratory showed that diabetes increases platelet aggregation in rats, but only in washed platelets. In the present study, we evaluated platelet aggregation coupled with adenosine triphosphate (ATP) release in normal and diabetic rats using a whole blood electrical aggregometer. Additionally, we investigated the role of endothelium-derived relaxing factor, or nitric oxide, in the platelet reactivity in diabetic rats. Rats were made diabetic using streptozocin, 55 mg/kg. After 1 month the rats were anesthetized, and arterial blood samples were collected directly into sodium citrate solution 3.8%. Platelet counts and mean platelet volumes were determined. Platelet aggregation, disaggregation, and ATP release in response to adenosine diphosphate (ADP), collagen, and arachidonic acid were measured. Platelet aggregation in response to ADP, collagen, and arachidonic acid was not different in diabetic rats when compared with that in controls. However, ATP release in response to ADP was significantly increased in diabetic rats. Platelets from diabetic animals were significantly larger than those of controls. Nitro-L-arginine methyl ester, a nitric oxide synthase inhibitor, decreased platelet aggregation in response to ADP in the normal animals, but not in the diabetic animals. However, arginine-induced nitric oxide production decreased platelet aggregation and enhanced the occurrence of disaggregation in platelets from both normal and diabetic rats. From these studies, we conclude that platelet aggregation in diabetic rats is not different using whole blood electrical aggregation, but platelet ATP secretion is significantly enhanced. Additionally, nitric oxide may modulate the platelet aggregation, disaggregation, and ATP secretory response. However, it does not appear to be a major factor in the altered aggregation responses in diabetic rats.
我们实验室之前的研究表明，糖尿病会增加大鼠血小板的聚集，但仅在洗涤过的血小板中出现这种情况。在本研究中，我们使用全血电凝集仪评估了正常大鼠和糖尿病大鼠中血小板聚集与三磷酸腺苷（ATP）释放的情况。此外，我们研究了内皮源性舒张因子或一氧化氮在糖尿病大鼠血小板反应性中的作用。使用链脲佐菌素（55mg/kg）使大鼠患糖尿病。1个月后，将大鼠麻醉，并将动脉血样本直接采集到3.8%的柠檬酸钠溶液中。测定血小板计数和平均血小板体积。测量血小板对二磷酸腺苷（ADP）、胶原和花生四烯酸的聚集、解聚及ATP释放情况。与对照组相比，糖尿病大鼠对ADP、胶原和花生四烯酸的血小板聚集无差异。然而，糖尿病大鼠对ADP的ATP释放显著增加。糖尿病动物的血小板明显大于对照组。一氧化氮合酶抑制剂硝基-L-精氨酸甲酯可降低正常动物对ADP的血小板聚集，但对糖尿病动物无效。然而，精氨酸诱导的一氧化氮生成可降低正常和糖尿病大鼠血小板的聚集，并增强血小板解聚的发生。从这些研究中，我们得出结论，使用全血电凝集法时，糖尿病大鼠的血小板聚集无差异，但血小板ATP分泌显著增强。此外，一氧化氮可能调节血小板聚集、解聚及ATP分泌反应。然而，它似乎不是糖尿病大鼠聚集反应改变的主要因素。
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