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首页> 外文期刊>American Journal of Physiology >Nitroglycerin reduces myocardial oxygen consumption during exercise despite vascular tolerance.
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Nitroglycerin reduces myocardial oxygen consumption during exercise despite vascular tolerance.

机译：尽管有血管耐受性，硝酸甘油仍可减少运动过程中的心肌耗氧量。

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摘要

The long-term benefits of nitroglycerin (NTG) therapy are limited by the development of vascular tolerance and endothelial dysfunction in conductance coronary arteries. We have determined whether nitrate tolerance extends to NTG effects on myocardial O2 consumption (MV(O2)) and the ability of endogenous nitric oxide (NO) to modulate MV(O2) during exercise. In chronically instrumented dogs (n = 8), hemodynamic and MV(O2) responses to treadmill exercise were measured before, during tolerance (3 and 7 days of NTG delivery), and 7 days after NTG withdrawal. Acute NTG delivery caused a parallel downward shift of the MV(O2)-triple product (TP) relations and reversed the disproportionate increases in MV(O2) caused by the blockade of NO formation. After 7 days of continuous transdermal NTG delivery, vascular tolerance was displayed as a >75% reduction of coronary blood flow (CBF) responses to NTG boluses. Despite vascular nitrate tolerance, MV(O2)-TP relations were shifted downward compared with pre-NTG exercise. Seven days after NTG withdrawal, vascular responses to boluses of NTG had recovered from tolerance, and MV(O2)-TP relations during exercise were back to pre-NTG level. At that time, blockade of NO formation failed to alter MV(O2)-TP relations. Thus NTG caused a sustained reduction of cardiac MV(O2), independent of metabolic demand during exercise, despite tolerance of the coronary microcirculation. NTG-induced vascular tolerance and MV(O2) reductions were reversible by NTG withdrawal, but endogenous NO-dependent modulation of O2 consumption was severely impaired.
机译：硝酸甘油（NTG）治疗的长期益处受到电导冠状动脉中血管耐受性和内皮功能障碍的发展的限制。我们已经确定硝酸盐耐受性是否扩展到NTG对心肌O2消耗（MV（O2））的影响以及运动过程中内源性一氧化氮（NO）调节MV（O2）的能力。在长期使用仪器的狗（n = 8）中，在耐受之前（NTG分娩的3天和7天）和NTG停药后7天，测量了对跑步机运动的血流动力学和MV（O2）反应。急性NTG传递引起MV（O2）-三重积（TP）关系的平行向下移动，并逆转了由NO形成的封锁引起的MV（O2）的不成比例的增加。连续透皮NTG递送7天后，血管耐受性显示为对NTG推注的冠状动脉血流量（CBF）降低> 75％。尽管对血管硝酸盐具有耐受性，但与NTG前运动相比，MV（O2）-TP关系向下移动。 NTG撤药后7天，对NTG推注的血管反应已从耐受性恢复，运动期间的MV（O2）-TP关系恢复到NTG之前的水平。当时，NO形成的封锁未能改变MV（O2）-TP关系。因此，尽管冠状动脉微循环耐受，NTG仍导致心脏MV（O2）持续降低，与运动期间的代谢需求无关。 NTG撤药可逆转NTG诱导的血管耐受性和MV（O2）降低，但严重损害了内源性NO依赖的O2消耗调节。

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