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首页> 外文期刊>American Journal of Physiology >Nitric oxide production is maintained in exercising swine with chronic left ventricular dysfunction.
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Nitric oxide production is maintained in exercising swine with chronic left ventricular dysfunction.

机译：锻炼患有慢性左心功能不全的猪可维持一氧化氮的产生。

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摘要

Left ventricular (LV) dysfunction caused by myocardial infarction (MI) is accompanied by endothelial dysfunction, most notably a loss of nitric oxide (NO) availability. We tested the hypothesis that endothelial dysfunction contributes to impaired tissue perfusion during increased metabolic demands as produced by exercise, and we determined the contribution of NO to regulation of regional systemic, pulmonary, and coronary vasomotor tone in exercising swine with LV dysfunction produced by a 2- to 3-wk-old MI. LV dysfunction resulted in blunted systemic and coronary vasodilator responses to ATP, whereas the responses to nitroprusside were maintained. Exercise resulted in blunted systemic and pulmonary vasodilator responses in MI that resembled the vasodilator responses in normal (N) swine following blockade of NO synthase with N(omega)-nitro-L-arginine (L-NNA, 20 mg/kg iv). However, L-NNA resulted in similar decreases in systemic (43 +/- 3% in N swine and 49 +/- 4% in MI swine), pulmonary (45 +/- 5% in N swine and 49 +/- 4% in MI swine), and coronary (28 +/- 4% in N and 35 +/- 3% in MI) vascular conductances in N and MI swine under resting conditions; similar effects were observed during treadmill exercise. Selective inhibition of inducible NO synthase with aminoguanidine (20 mg/kg iv) had no effect on vascular tone in MI. These findings indicate that while agonist-induced vasodilation is already blunted early after myocardial infarction, the contribution of endothelial NO synthase-derived NO to regulation of vascular tone under basal conditions and during exercise is maintained.
机译：由心肌梗塞（MI）引起的左心室（LV）功能障碍伴有内皮功能障碍，最明显的是一氧化氮（NO）可用性降低。我们测试了运动功能引起的代谢需求增加期间内皮功能障碍导致组织灌注受损的假说，并确定了NO对运动猪产生的LV功能障碍所致的区域性全身，肺和冠状血管舒张压的调节作用。 -3周前的MI。左室功能不全导致对ATP的全身和冠状血管舒张反应减弱，而对硝普钠的反应得以维持。运动导致MI中全身和肺血管舒张反应减弱，类似于正常（N）猪在用N（ω）-硝基-L-精氨酸（L-NNA，20 mg / kg iv）阻断NO合酶后的血管舒张反应。然而，L-NNA导致全身性下降（N猪为43 +/- 3％，MI猪为49 +/- 4％），肺部（N猪为45 +/- 5％，N猪为49 +/- 4在静息状态下，N和MI猪的冠状血管电导（在MI猪中为％），在N和MI猪中为冠状动脉（N在28 +/- 4％，MI在35 +/- 3％）;在跑步机锻炼期间也观察到类似的效果。氨基胍（20 mg / kg iv）对诱导型NO合酶的选择性抑制对MI的血管张力没有影响。这些发现表明，尽管在心肌梗塞后激动剂引起的血管舒张作用已经减弱，但在基础条件下和运动过程中，内皮一氧化氮合酶衍生的一氧化氮在调节血管紧张中的作用仍然得以维持。

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