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首页> 外文期刊>American Journal of Physiology >Sustained hypothermia accelerates microvascular thrombus formation in mice.
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Sustained hypothermia accelerates microvascular thrombus formation in mice.

机译：持续的低温会加速小鼠微血管血栓的形成。

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摘要

Cold is supposed to be associated with alterations in blood coagulation and a pronounced risk for thrombosis. We studied the effect of clinically encountered systemic hypothermia on microvascular thrombosis in vivo and in vitro. Ferric chloride-induced microvascular thrombus formation was analyzed in cremaster muscle preparations from hypothermic mice. Additionally, flow cytometry and Western blot analysis was used to evaluate the effect of hypothermia on platelet activation. To test whether preceding hypothermia predisposes for enhanced thrombosis, experiments were repeated after hypothermia and rewarming to 37 degrees C. Control animals revealed complete occlusion of arterioles and venules after 742 +/- 150 and 824 +/- 172 s, respectively. Systemic hypothermia of 34 degrees C accelerated thrombus formation in arterioles and venules (279 +/- 120 and 376 +/- 121 s; P < 0.05 vs. 37 degrees C). This was further pronounced after cooling to 31 degrees C (163 +/- 57 and 281 +/- 71 s; P < 0.05 vs. 37 degreesC). Magnitude of thrombin receptor activating peptide (TRAP)-induced platelet activation increased with decreasing temperatures, as shown by 1.8- and 3.0-fold increases in mean fluorescence after PAC-1 binding to glycoprotein (GP)IIb-IIIa and 1.6- and 2.9-fold increases of fibrinogen binding on incubation at 34 degrees C and 31 degrees C. Additionally, tyrosine-specific protein phosphorylation in platelets was increased at hypothermic temperatures. In rewarmed animals, kinetics of thrombus formation were comparable to those in normothermic controls. Concomitantly, spontaneous and TRAP-enhanced GPIIb-IIIa activation did not differ between rewarmed platelets and those maintained continuously at 37 degrees C. Moderate systemic hypothermia accelerates microvascular thrombosis, which might be mediated by increased GPIIb-IIIa activation on platelets but does not cause predisposition with increased risk for microvascular thrombus formation after rewarming.
机译：感冒可能与凝血功能改变和明显的血栓形成风险有关。我们研究了体内和体外临床遇到的体温过低对微血管血栓形成的影响。在低温小鼠的提睾肌制剂中分析了氯化铁诱导的微血管血栓形成。另外，使用流式细胞仪和蛋白质印迹分析来评估体温过低对血小板活化的影响。为了测试先前的体温过高是否容易导致血栓形成，在体温过低并重新升温至37摄氏度后重复实验。对照动物分别在742 +/- 150和824 +/- 172 s后分别显示出小动脉和小静脉完全闭塞。 34°C的全身性体温过低会加速小动脉和小静脉中的血栓形成（279 +/- 120和376 +/- 121 s; P <0.05对37摄氏度）。冷却至31摄氏度（163 +/- 57和281 +/- 71 s; P <0.05对37摄氏度）后，这一点更加明显。凝血酶受体活化肽（TRAP）诱导的血小板活化程度随温度降低而增加，如PAC-1与糖蛋白（GP）IIb-IIIa和1.6-和2.9-结合后平均荧光增加1.8和3.0倍所示在34℃和31℃下孵育时，纤维蛋白原结合的结合增加了3倍。另外，在低温下，血小板中酪氨酸特异性蛋白的磷酸化增加了。在温热的动物中，血栓形成的动力学与正常体温对照的相当。同时，自重和TRAP增强的GPIIb-IIIa活化在重新温热的血小板和持续维持在37°C的血小板之间没有差异。中度的体温过低会加速微血管血栓形成，这可能是由血小板上GPIIb-IIIa活化的增加所介导的，但不会引起易感性复温后增加微血管血栓形成的风险。

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