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尿毒症会影响血小板膜流动性和血小板内钙离子动员。

Platelet membrane fluidity and intraplatelet Ca2+ mobilization are affected in uraemia.

作者信息

Walkowiak B, Borkowska E, Koziolkiewicz W, Michalec L, Sobol A, Cierniewski C S

机构信息

Department of Biophysics, Medical University of Lodz, Poland.

出版信息

Eur J Haematol. 1997 May;58(5):350-6. doi: 10.1111/j.1600-0609.1997.tb01682.x.

Abstract

In present investigations, platelet membrane fluidity and intraplatelet Ca2+ mobilization were analysed in uraemic platelets by fluorescence techniques. Thirteen non-dialyzed uraemic patients and 16 control subjects were examined. Anisotropy of DPH-probe, measured at 37 degrees C, was significantly higher in control (0.2236 +/- 0.0050) than in uraemic platelets (0.1969 +/- 0.0082; p < 0.01). There was no difference between control (109.8 +/- 6.0 nM) and uraemic platelets (100.0 +/- 7.3 nM) when the basal [Ca2+]i in resting platelets was determined. Activation of platelets by ADP (12.5 microM) or by thrombin (0.1 U/ml) resulted in an increase in [Ca2+]i. It was significantly higher (p* < 0.003 for ADP and p* < 0.009 for thrombin, respectively) in control platelets (383.6 +/- 56.3 nM and 2031.0 +/- 298.8 nM, respectively) than in uraemic ones (191.0 +/- 21.3 nM and 838.7 +/- 144.1 nM, respectively). The amount of released Ca2+ was higher in control platelets activated by both ADP and thrombin (157.6 +/- 21.4 nM and 409.3 +/- 71.0 nM, respectively) than in uraemic platelets (76.7 +/- 15.7 nM and 203.0 +/- 29.3 nM, respectively) and the differences were significant (p < 0.01 and p* < 0.01, respectively). These results indicate an abnormal intracellular Ca2+ mobilization in uraemic platelets. Both increased membrane fluidity and decreased Ca2+ mobilization should be considered as a possible reason of reduced fibrinogen receptor exposure on uraemic platelets.

摘要

在目前的研究中,采用荧光技术分析了尿毒症患者血小板的膜流动性和血小板内钙离子动员情况。研究了13例未透析的尿毒症患者和16例对照者。在37℃下测量的DPH探针各向异性,对照组(0.2236±0.0050)显著高于尿毒症血小板组(0.1969±0.0082;p<0.01)。测定静息血小板的基础[Ca2+]i时,对照组(109.8±6.0 nM)和尿毒症血小板组(100.0±7.3 nM)之间无差异。ADP(12.5 microM)或凝血酶(0.1 U/ml)激活血小板会导致[Ca2+]i升高。对照组血小板(分别为383.6±56.3 nM和2031.0±298.8 nM)中的升高幅度显著高于尿毒症血小板组(分别为191.0±21.3 nM和838.7±144.1 nM)(ADP时p*<0.003,凝血酶时p*<0.009)。ADP和凝血酶激活的对照组血小板中释放的Ca2+量(分别为157.6±21.4 nM和409.3±71.0 nM)高于尿毒症血小板组(分别为76.7±15.7 nM和203.0±29.3 nM),差异具有统计学意义(分别为p<0.01和p*<0.01)。这些结果表明尿毒症血小板存在细胞内钙离子动员异常。膜流动性增加和钙离子动员减少均应被视为尿毒症血小板上纤维蛋白原受体暴露减少的可能原因。

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