Gaudard A, Varlet-Marie E, Monnier J F, Janbon Ch, Quéré I, Bressolle F, Brun J-F
Laboratoire de Pharmacocinétique Clinique, Faculté de Pharmacie, Université Montpellier I, France.
Clin Hemorheol Microcirc. 2002;27(2):115-22.
Exercise-induced impairment in blood fluidity has been supposed to increase cardiovascular risk but there is no data to support this hypothesis. We report the case of a 50 yr old marathon runner who underwent a central retinal vein thrombosis after a marathon run. We investigated his rheological response to exercise compared to control subjects of previous studies. During a standardized sub-maximal exercise-test, the increase in blood viscosity (+28%) and hematocrit (+25%) exceeded the control range but the most striking differences were found for red cell aggregation (Myrenne +47%) and disaggregation thresholds (Affibio +37%). Although some of this post-exercise hyperviscosity pattern may be due to the previous vascular event, these findings may also support the hypothesis of a role for hemorheological alterations during exercise in the pathogenesis of this marathon-induced retinal thrombosis, and indicate that after such an event hemorheological adaptation to exercise remains markedly disturbed.
运动引起的血液流动性受损被认为会增加心血管风险，但尚无数据支持这一假设。我们报告了一名50岁马拉松运动员在跑完马拉松后发生视网膜中央静脉血栓形成的病例。与先前研究的对照受试者相比，我们调查了他对运动的流变学反应。在标准化的次最大运动测试中，血液粘度增加（+28%）和血细胞比容增加（+25%）超过了对照范围，但红细胞聚集（Myrenne +47%）和解聚阈值（Affibio +37%）的差异最为显著。尽管运动后这种高粘度模式的一部分可能归因于先前的血管事件，但这些发现也可能支持这样一种假设，即运动期间血液流变学改变在这种马拉松诱发的视网膜血栓形成的发病机制中起作用，并表明在发生此类事件后，血液流变学对运动的适应性仍然明显受到干扰。
