Micromechanics Control of Coronary Circulation

我们组织这个跨学科的项目是为了从冠状血管和心肌之间的机械-能量相互作用的角度更好地了解冠状动脉微循环的调节。以下是本项目的主要发现。借助针-探头CCD活体显微镜和冠状动脉灌注系统，我们评估了冠状动脉对冠状动脉灌注压力降低的反应。当冠状动脉灌注压降低时，小动脉的小脉冲星横贯压力可能导致小动脉扩张。内皮源性超极化因子主要作用于小冠状动脉的扩张，而一氧化氮主要作用于大冠状动脉和小冠状动脉的扩张。当这些机制被抑制时，腺苷和二氧化碳可能在冠状动脉扩张中起代偿作用。当降低灌注压降低冠状动脉血流时，舒张时间分数升高。舒张时间分数的调节可以为血管舒张储备衰竭时心肌的供需匹配提供重要的调节机制。利用波强度评价机械心血管耦合对心脏性能变化敏感，可用于评价机械对冠状动脉循环的影响。利用分子血流示踪剂在毛细管水平上对血流分布进行显微成像，有助于评价冠状动脉微循环的机械能量调节。Β1-Adrenoceptor阻断降低了心内膜下灌注的微观异质性。一氧化氮供体抑制流动（剪切应力）诱导的一氧化氮的产生。四氢生物蝶呤可能抵消一氧化氮供体介导的抑制。间隙连接可能在微血管调控中发挥异细胞通讯的作用。

We organized this interdisciplinary project in order to provide a better understanding of the regulation of coronary microcirculation from a viewpoint of mechanoenergetic interaction between coronary vessels and myocardium. Followings are the major findings from this project.With aids of needle-probe CCD intravital microscopy and coronary perfusion system, we evaluated the behavior of the coronary arterioles in response to a reduction of coronary perfusion pressure. Pulsatilet ransmural pressure of the arterioles may contribute to the arteriolar dilation in response to a decrease in coronary perfusion pressure. Endothelium-derived hyperpolarizing factor contributes mainly to the dilation of the smaller coronary arteriole, while nitric oxide of the lager coronary arteriole and the smaller artery. When these mechanisms are inhibited, adenosine and Pco2 may play compensatory role in the coronary arteriolar dilation.Diastolic time fraction increased when coronary flow was reduced by lowering perfusion pressure. Modulation of the diastolic time fraction can provide an important regulatory mechanism to match supply and demand of the myocardium when vasodilatory reserve is exhausted.Evaluation of mechanical cardiovascular coupling using the wave intensity is sensitive to the change in cardiac performance and may be applicable to the evaluation of the mechanical effects to the coronary circulation.Micro-imaging of the blood flow distribution at capillary level using molecular flow tracer is useful for evaluating mechanoenergetic regulation of coronary microcirculatiom. Β1-Adrenoceptor blockade reduced microheterogeneity of the subendocardial perfusion.Nitric oxide donor suppressed the flow (shear stress)-induced production of nitric oxide. Tetrahydrobiopterin may counteract the nitric oxide donor-mediated suppression. Gap junctions may play a role in heterocellular communication in the microvascular regulation.