Symons J D, Rendig S V, Stebbins C L, Longhurst J C
Department of Internal Medicine, Division of Cardiovascular Medicine, University of California, Davis 95616, USA.
J Appl Physiol (1985). 2000 Feb;88(2):433-42. doi: 10.1152/jappl.2000.88.2.433.
We hypothesized that exercise training preserves endothelium-dependent relaxation, lessens receptor-mediated constriction of coronary resistance arteries, and reduces myocardial contractile dysfunction in response to ischemia. After 10 wk of treadmill running or cage confinement, regional and global indexes of left ventricular contractile function were not different between trained and sedentary animals in response to three 15-min periods of ischemia (long-term; n = 17), one 5-min bout of ischemia (short-term; n = 18), or no ischemia (sham-operated; n = 24). Subsequently, coronary resistance vessels ( approximately 106 +/- 4 microm ID) were isolated and studied using wire myographs. Maximal ACh-evoked relaxation was approximately 25, 40, and 60% of KCl-induced preconstriction after the long-term, short-term, and sham-operated protocols, respectively, and was similar between groups. Maximal sodium nitroprusside-evoked relaxation also was similar between groups among all protocols, and vasoconstrictor responses to endothelin-1 and U-46619 were not different in trained and sedentary rats after short-term ischemia or sham operation. We did observe that, after long-term ischemia, maximal tension development in response to endothelin-1 and U-46619 was blunted (P < 0.05) in trained animals by approximately 70 and approximately 160%, respectively. These results support our hypothesis that exercise training lessens receptor-mediated vasoconstriction of coronary resistance vessels after ischemia and reperfusion. However, training did not preserve endothelial function of coronary resistance vessels, or myocardial contractile function, after ischemia and reperfusion.
我们假设运动训练可维持内皮依赖性舒张，减轻受体介导的冠状动脉阻力血管收缩，并减少缺血引起的心肌收缩功能障碍。在进行10周的跑步机跑步或笼养后，在经历三个15分钟的缺血期（长期；n = 17）、一个5分钟的缺血发作（短期；n = 18）或无缺血（假手术；n = 24）的情况下，训练组和久坐组动物的左心室收缩功能的局部和整体指标并无差异。随后，分离出冠状动脉阻力血管（内径约106 +/- 4微米），并使用线肌动描记器进行研究。在长期、短期和假手术方案后，乙酰胆碱诱发的最大舒张分别约为氯化钾诱发的预收缩的25%、40%和60%，且各组之间相似。在所有方案中，硝普钠诱发的最大舒张在各组之间也相似，并且在短期缺血或假手术后，训练组和久坐组大鼠对内皮素-1和U-46619的血管收缩反应并无差异。我们确实观察到，在长期缺血后，训练组动物对内皮素-1和U-46619的最大张力发展分别减弱了约70%和约160%（P < 0.05）。这些结果支持了我们的假设，即运动训练可减轻缺血再灌注后受体介导的冠状动脉阻力血管收缩。然而，训练并未在缺血再灌注后维持冠状动脉阻力血管的内皮功能或心肌收缩功能。
