Jagiellonian Centre for Experimental Therapeutics (JCET), Jagiellonian University, Krakow, POLAND.
Department of Muscle Physiology, Chair of Physiology and Biochemistry, Faculty of Rehabilitation, University School of Physical Education, Krakow, POLAND.
Med Sci Sports Exerc. 2018 Jul;50(7):1405-1412. doi: 10.1249/MSS.0000000000001589.
An acute bout of strenuous exercise in humans results in transient impairment of nitric oxide (NO)-dependent function, but it remains unknown whether this phenomenon is associated with increased risk of thrombotic events after exercise. This study aimed to evaluate effects of a single bout of exhaustive running in mice on the balance of vascular NO/reactive oxygen species production, and on thrombogenicity.
At different time points (0, 2, and 4 h) after exercise and in sedentary C57BL/6 mice, the production of NO and superoxide (O2) in aorta was measured by electron paramagnetic resonance spin trapping and by dihydroethidium/high-performance liquid chromatography-based method, respectively, whereas collagen-induced thrombus formation was analyzed in a microchip-based flow-chamber system (total thrombus-formation analysis system). We also measured pre- and postexercise plasma concentration of nitrite/nitrate and 6-keto-PGF1α.
An acute bout of exhaustive running in mice resulted in decreased production of NO and increased production of O2 in aorta, with maximum changes 2 h after completion of exercise when compared with sedentary mice. However, platelet thrombus formation was not changed by exercise as evidenced by unaltered time to start of thrombus formation, capillary occlusion time, and total thrombogenicity (area under the flow pressure curve) as measured in a flow-chamber system. Strenuous exercise increased the plasma concentration of nitrite but did not affect nitrate and 6-keto-PGF1α concentrations.
An acute bout of strenuous exercise in mice reduced NO and in parallel increased O2 production in aorta. This response was most pronounced 2 h after exercise. Surprisingly, the reduced NO and increased O2 production in mice after exercise did not result in increased platelet-dependent thrombogenicity. These results show that transient reduction in NO bioavailability does not modify thromboresistance in healthy mice after exercise.
人类剧烈运动后会出现短暂的一氧化氮(NO)依赖功能障碍,但目前尚不清楚这种现象是否与运动后血栓形成事件的风险增加有关。本研究旨在评估一次性剧烈运动对小鼠血管 NO/活性氧产生平衡和血栓形成的影响。
在运动后不同时间点(0、2 和 4 小时)和安静的 C57BL/6 小鼠中,通过电子顺磁共振自旋捕集法和二氢乙啶/高效液相色谱法分别测量主动脉中 NO 和超氧阴离子(O2)的产生,并用微芯片流式室系统(全血栓形成分析系统)分析胶原诱导的血栓形成。我们还测量了运动前后血浆中亚硝酸盐/硝酸盐和 6-酮-PGF1α的浓度。
一次性剧烈运动导致小鼠主动脉中 NO 的产生减少和 O2 的产生增加,与安静小鼠相比,运动后 2 小时时变化最大。然而,运动并没有改变血小板血栓形成,因为在流式室系统中测量的血栓形成开始时间、毛细血管阻塞时间和总血栓形成性(血流压力曲线下面积)没有改变。剧烈运动增加了血浆中亚硝酸盐的浓度,但不影响硝酸盐和 6-酮-PGF1α的浓度。
一次性剧烈运动使小鼠主动脉中 NO 减少,同时 O2 的产生增加。这种反应在运动后 2 小时最为明显。令人惊讶的是,运动后小鼠中 NO 和 O2 产生的减少并没有导致血小板依赖性血栓形成性增加。这些结果表明,健康小鼠运动后短暂的 NO 生物利用度降低不会改变其抗血栓性。