首页> 外文期刊>American Journal of Physiology >Alterations of endothelium-dependent and -independent regulation of coronary blood flow during heart failure.
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Alterations of endothelium-dependent and -independent regulation of coronary blood flow during heart failure.

机译:心力衰竭期间对冠状动脉血流的内皮依赖性和非依赖性调节的改变。

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Conflicting data concerning the changes in basal coronary blood flow and nitric oxide (NO)-releasing capacity in chronic heart failure may be due to different phases or duration of heart failure. To investigate endothelium-dependent and -independent regulation of coronary blood flow in different phases of heart failure, coronary pressure-flow relationships during long diastole were obtained before and after rapid pacing of 3 and 5 wk at 240 beats/min in 12 or 6 dogs. Neither basal coronary blood flow nor the slope of coronary pressure-flow relationships changed; however, zero-flow pressure increased slightly after rapid pacing. Intracoronary injection of N(G)-nitro-L-arginine methyl ester decreased coronary blood flow at a perfusion pressure of 50 mmHg by approximately 20% at baseline, 55% after 3 wk of rapid pacing, and 20% after 5 wk of rapid pacing. Acetylcholine-induced increase in coronary blood flow was maintained for 3 wk but was finally attenuated after 5 wk of rapid pacing. In contrast, the coronary blood flow response to adenosine gradually decreased with time. These results suggest that basal coronary blood flow is maintained until the late stage of heart failure, presumably by an increases in NO production during the early stage and then by other vasodilatory substances during the late stage, and that endothelium-dependent vasodilation via exogenously administered acetylcholine in resistance vessels is not necessarily impaired in the early stage despite the gradual reduction of endothelium-independent vasodilation via adenosine in chronic heart failure.
机译:有关慢性心力衰竭患者基础冠状动脉血流变化和一氧化氮释放能力的数据不一致,可能是由于心力衰竭的不同阶段或持续时间所致。为了研究心力衰竭不同阶段中内皮依赖性和非依赖性的冠状动脉血流调节,在12或6只狗以240次/ min的速度快速起搏3和5周时,在长舒张期期间获得了冠脉压力与血流的关系。 。冠状动脉基础血流量和冠脉压力-流量关系的斜率都没有改变;但是,快速起搏后,零流量压力略有增加。冠状动脉内注射N(G)-硝基-L-精氨酸甲酯可在50 mmHg的灌注压力下使基线时的冠状动脉血流量减少约20%,在快速起搏3周后降低55%,在快速起搏3周后降低20%起搏。乙酰胆碱引起的冠状动脉血流增加维持3周,但在5周快速起搏后最终减弱。相反,冠状动脉对腺苷的血流反应随时间逐渐降低。这些结果表明,基础冠状动脉血流一直维持到心力衰竭的晚期,大概是由于早期阶段NO的增加,然后是后期阶段的其他血管舒张物质的增加,以及通过外源性乙酰胆碱引起的内皮依赖性血管舒张尽管在慢性心力衰竭中通过腺苷逐渐减少了非内皮依赖性血管舒张,但在早期阻力血管中的抗癌药物并不一定受损。

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