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首页> 外文期刊>American Journal of Physiology >Contribution of KATP+ channels to coronary vasomotor tone regulation is enhanced in exercising swine with a recent myocardial infarction.
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Contribution of KATP+ channels to coronary vasomotor tone regulation is enhanced in exercising swine with a recent myocardial infarction.

机译：在运动有近期心肌梗塞的猪时，KATP +通道对冠状动脉血管舒缩张力调节的贡献得到增强。

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Previous studies demonstrated a decreased flow reserve in the hypertrophied myocardium early after myocardial infarction (MI). Previously, we reported that exacerbation of hemodynamic abnormalities and neurohumoral activation during exercise caused slight impairment of myocardial O(2) supply in swine with a recent MI. We hypothesized that increased metabolic coronary vasodilation [via ATP-sensitive K(+) (K(ATP)(+)) channels and adenosine] may have partially compensated for the increased extravascular compressive forces and increased vasoconstrictor neurohormones, thereby preventing a more severe impairment of myocardial O(2) balance. Chronically instrumented swine were exercised on a treadmill up to 85% of maximum heart rate. Under resting conditions, adenosine receptor blockade [8-phenyltheophylline (8-PT), 5 mg/kg i.v.] and K(ATP)(+) channel blockade (glibenclamide, 3 mg/kg i.v.) produced similar decreases in myocardial O(2) supply in normal and MI swine. However, while glibenclamide's effect waned in normal swine during exercise (P < 0.05), it was maintained in MI swine. 8-PT's effect was maintained during exercise and was not different between normal and MI swine. Finally, in normal swine combined treatment with 8-PT and glibenclamide produced a vasoconstrictor response that equaled the sum of the responses to blockade of the individual pathways. In contrast, in MI swine the vasoconstrictor response to 8-PT and glibenclamide was similar to that produced by glibenclamide alone. In conclusion, despite significant hemodynamic abnormalities in swine with a recent MI, myocardial O(2) supply and O(2) consumption in remodeled myocardium are still closely matched during exercise. This close matching is supported by increased K(ATP)(+) channel-mediated coronary vasodilation. Although the net vasodilator influence of adenosine was unchanged in remodeled myocardium, it became exclusively dependent on K(ATP)(+) channel opening.
机译：先前的研究表明，心肌梗塞（MI）早期，肥厚型心肌的血流储备减少。以前，我们报道，运动期间血液动力学异常和神经体液激活的加剧导致猪近期心肌梗死对心肌O（2）的供应造成轻微损害。我们假设增加的代谢性冠状动脉血管舒张[通过ATP敏感的K（+）（K（ATP）（+））通道和腺苷]可能部分补偿了血管外压缩力的增加和血管收缩神经激素的增加，从而防止了更严重的损伤O（2）平衡在跑步机上锻炼慢性仪器化的猪，最高可达到最大心率的85％。在静止状态下，腺苷受体阻滞剂[8-苯基茶碱（8-PT），5 mg / kg iv]和K（ATP）（+）通道阻滞剂（glibenclamide，3 mg / kg iv）产生相似的心肌O（2）降低。 ）供应正常和MI猪。然而，尽管在运动期间正常猪中格列本脲的作用减弱（P <0.05），但在MI猪中却保持了。运动过程中维持了8-PT的作用，正常猪和MI猪之间没有差异。最后，在正常猪中，用8-PT和格列本脲联合治疗产生的血管收缩反应等于对单个途径阻断反应的总和。相反，在MI猪中，对8-PT和格列本脲的血管收缩反应与单独使用格列本脲产生的反应相似。总之，尽管猪近期出现严重的血液动力学异常，但运动过程中心肌的O（2）供应和O（2）消耗在重塑的心肌中仍然紧密匹配。 K（ATP）（+）通道介导的冠状动脉血管舒张增加支持了这种紧密匹配。尽管腺苷的净血管扩张剂影响在重构的心肌中没有改变，但它完全取决于K（ATP）（+）通道的开放。

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