Micromechanics Control of Coronary Circulation

我们组织了这个跨学科的项目，以提供一个更好地了解冠状动脉微循环的调节，从冠状动脉血管和心肌之间的机械能相互作用的观点。本研究的主要结果如下：我们借助针探头CCD活体显微镜和冠状动脉灌注系统，评价了冠状动脉对冠状动脉灌注压降低的反应。小动脉的搏动性跨壁压可能有助于响应于冠状动脉灌注压降低的小动脉扩张。内皮源性超极化因子主要参与冠状小动脉的扩张，而一氧化氮主要参与冠状大动脉和小动脉的扩张。当这些机制被抑制时，腺苷和Pco2可能在冠状动脉扩张中起代偿作用，降低灌注压减少冠脉流量时，舒张时间分数增加。舒张期时间分数的调节是舒张功能衰竭时心肌供需平衡的重要调节机制，利用波强度评价心血管机械耦合对心功能变化敏感，可用于评价冠状动脉循环的机械效应。用分子流示踪剂对毛细血管水平的血流分布成像可用于评价冠状动脉微循环的机械能调节。阻断Β_1肾上腺素能受体可减少内皮下灌注的微不均匀性，一氧化氮供体可抑制血流（剪切应力）诱导的一氧化氮产生。四氢生物蝶呤可能会抵消一氧化氮供体介导的抑制。缝隙连接可能在微血管调节中起异源细胞通讯的作用。

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.