Micromechanics Control of Coronary Circulation

冠状动脉循环的微力学控制

• 批准号: 10044330
• 负责人: KAJIYA Fumihiko
• 金额: $ 6.98万
• 依托单位: Kawasaki Medical School
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (A).
• 财政年份: 1998
• 资助国家: 日本
• 起止时间: 1998 至 1999
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-10044330/
• 关键词: coronary microcirculation; blood flow regulation; mechanical stress; myocardial ischemia; molecular flow tracer; vascular response; 血管反応; 冠微少循環

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.

我们组织这一跨学科的项目是为了从冠脉和心肌之间的机械能相互作用的角度更好地理解冠脉微循环的调节。以下是该项目的主要发现。借助针头-探针式电荷耦合器件活体显微镜和冠状动脉灌注系统，我们评估了冠状动脉小动脉对冠脉灌注压降低的反应。小动脉的脉搏波壁压可能与冠脉灌流压降低所致的微动脉扩张有关。内皮源性超极化因子主要促进冠状动脉小动脉的扩张，而大冠状动脉和小动脉的一氧化氮则主要起作用。当这些机制被抑制时，腺苷和二氧化碳可能在冠状动脉小动脉扩张中起到代偿作用。当降低灌流压减少冠脉流量时，舒张期时间分数增加。当血管扩张储备耗尽时，舒张期时间分数的调节可以为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的变化敏感，可用于评价机械效应对冠状动脉循环的影响。利用分子流示踪剂在毛细血管水平上进行血流分布的显微成像有助于评价冠脉微循环的机械能调节。Β1受体阻断剂减少心内膜下灌流的微观异质性。一氧化氮供体抑制血流(切应力)诱导的一氧化氮的产生。四氢生物蝶呤可拮抗一氧化氮供体介导的抑制作用。缝隙连接可能在微血管调节的异质细胞通讯中发挥作用。

项目成果

Toyotaka Yada, et al.: "Role of NO and K+ATP channels in adenosine-induced vasodilation on in vivo canine subendocardial arterioles"American Journal of Physiology. 277. H1931-H1939 (1999)

Toyotaka Yada 等人：“NO 和 K ATP 通道在腺苷诱导体内犬心内膜下小动脉血管舒张中的作用”美国生理学杂志。

Osamu Hiramatsu, et al.: "In vivo observations of the intramural arterioles and venules in beating canine hearts"Journal of Physiology. 509. 619-628 (1998)

Osamu Hiramatsu 等人：“跳动犬心脏壁内小动脉和小静脉的体内观察”生理学杂志。

Toyotaka Yada: "Role of NO and K^+_<ATP> channels in adenosine-induced vasodilation on in vivo canine suberdocardial arterioles"American Journal of Physiology. 277. H1931-H1939 (1999)

Toyotaka Yada：“NO 和 K^_<ATP> 通道在腺苷诱导体内犬心内膜下小动脉血管舒张中的作用”美国生理学杂志。

Daphne Merkus: "Prolonged diastolic time fraction protects myocardial perfusion when coronary blood flow is reduced"Circulation. 100. 75-81 (1999)

Daphne Merkus：“当冠状动脉血流量减少时，延长舒张期时间可以保护心肌灌注”循环。

Daphne Merkus et al.: "Prolonged diastolic time fraction protects myocardal perfusion when coronary blood flow is reduced"Circulation. 100. 75-81 (1999)

Daphne Merkus 等人：“当冠状动脉血流量减少时，延长舒张期时间可保护心肌灌注”循环。