Tschoepe D, Homberg M, Roesen P, Gries F A
Cellular Haemostasis Group, Heinrich Heine University, Düsseldorf, FRG.
Diabetes Res. 1992 Mar;19(3):125-31.
Twenty-nine IDDM patients with borderline hypertension were randomly allocated to placebo or nitrendipine treatment. Nitrendipine was given orally at a dosage of 20 mg once daily over 4 weeks. Stimulated platelet thromboxane formation at rest and after standardized, non exhausting exercise was measured by standard methods. In addition, plasma levels of platelet factor 4 and aggregation responses to collagen and ADP were determined. In the treatment group thromboxane formation after stimulation with collagen (0.3 and 1.0 micrograms/ml) and 1 mM arachidonic acid (AA) was reduced in the resting state. Exercise induced change of thromboxane synthesis in response to 1.0 micrograms/ml collagen was significantly lower as compared to placebo (p < 0.05). In parallel, PF4 plasma levels were significantly lowered (p < 0.05). Whole blood aggregation after collagen stimulation (1.0 micrograms/ml) was reduced after 4 weeks of nitrendipine treatment, but ADP (5 microM) induced aggregation was not. These effects of nitrendipine were not seen in platelet rich plasma. In conclusion long-term nitrendipine treatment may inhibit collagen dependent platelet activation in the blood of diabetic patients with borderline hypertension.
29例患有临界高血压的胰岛素依赖型糖尿病(IDDM)患者被随机分配接受安慰剂或尼群地平治疗。尼群地平以每日20毫克的剂量口服,持续4周。通过标准方法测量静息状态下以及标准化、非耗尽性运动后的刺激血小板血栓素形成。此外,还测定了血小板因子4的血浆水平以及对胶原蛋白和二磷酸腺苷(ADP)的聚集反应。在治疗组中,静息状态下用胶原蛋白(0.3和1.0微克/毫升)和1毫摩尔花生四烯酸(AA)刺激后的血栓素形成减少。与安慰剂相比,运动诱导的对1.0微克/毫升胶原蛋白的血栓素合成变化显著更低(p < 0.05)。同时,血小板因子4的血浆水平显著降低(p < 0.05)。尼群地平治疗4周后,胶原蛋白刺激(1.0微克/毫升)后的全血聚集减少,但ADP(5微摩尔)诱导的聚集未减少。在富含血小板的血浆中未观察到尼群地平的这些作用。总之,长期尼群地平治疗可能抑制临界高血压糖尿病患者血液中胶原蛋白依赖性血小板活化。