Kajiya F, Tsujioka K, Ogasawara Y, Hiramatsu O, Wada Y, Goto M, Yanaka M
Department of Medical Engineering and Systems Cardiology, Kawasaki Medical School, Kurashiki, Japan.
Circ Res. 1989 Nov;65(5):1172-81. doi: 10.1161/01.res.65.5.1172.
To clarify the characteristics of the phasic blood velocity pattern in small arteries and veins on the left atrial surface, we used our newly developed fiber-optic laser Doppler velocimeter. We intended particularly to examine the influence of atrial contraction and relaxation on velocity waveforms to obtain some insight into the nature of the mechanical force acting on the atrial intramyocardial vascular beds. In 14 anesthetized open-chest dogs, the left atrial appendage was gently displaced to expose small branches of the artery and vein. Vessels with an outer diameter of about 150-500 microns were chosen for the measurements because their walls are transparent to laser light. The fiber tip (velocity sensor) was fixed on the vessel surface with a drop of cyanoacrylate when good-quality Doppler signals were consistently observed. Additional experiments with three dogs were performed to observe the blood velocities in the atrial artery and vein during arrhythmia. The blood velocity waveform in the artery was similar to the pattern of aortic pressure during ventricular ejection (peak velocity, 18.8 +/- 7.8 cm/sec) but was characterized by a pronounced dip during atrial contraction. The temporal coincidence between the dip formation and atrial contraction was confirmed during atrial flutter with an atrioventricular block. After isoproterenol administration (2 micrograms i.v.), the acceleration rate of the forward flow velocity increased by 176% (p less than 0.05), and reverse flow appeared during atrial contraction in five cases out of eight (p = 0.013). The blood flow velocity in atrial small veins, on the other hand, was predominant during atrial contraction (peak velocity, 15.6 +/- 5.8 cm/sec). Isoproterenol increased the acceleration rate of this forward flow velocity by 121% (p less than 0.01). Nitroglycerin did not change the blood velocity waveform significantly in atrial arteries or in veins. The phase opposition between arterial inflow into and venous outflow from the atrial myocardium indicates that a large portion of the coronary inflow to the atrial myocardium may be stored due to the presence of atrial myocardial vascular capacitance. We conclude that atrial myocardial contraction impedes atrial inflow and promotes venous outflow from atrial capacitance vessels.
为了阐明左心房表面小动脉和静脉的阶段性血流速度模式的特征，我们使用了新开发的光纤激光多普勒测速仪。我们特别旨在研究心房收缩和舒张对速度波形的影响，以深入了解作用于心房心肌内血管床的机械力的性质。在14只麻醉开胸犬中，轻轻移动左心耳以暴露动脉和静脉的小分支。选择外径约150 - 500微米的血管进行测量，因为它们的壁对激光是透明的。当持续观察到高质量的多普勒信号时，用一滴氰基丙烯酸酯将光纤尖端（速度传感器）固定在血管表面。另外对3只犬进行实验以观察心律失常时心房动脉和静脉中的血流速度。动脉中的血流速度波形类似于心室射血期间的主动脉压力模式（峰值速度，18.8±7.8厘米/秒），但其特征是在心房收缩期间有明显的下降。在伴有房室传导阻滞的心房扑动期间，证实了下降形成与心房收缩之间的时间一致性。静脉注射异丙肾上腺素（2微克）后，正向血流速度的加速率增加了176%（p< 0.05），并且在8例中有5例在心房收缩期间出现反向血流（p = 0.013）。另一方面，心房小静脉中的血流速度在心房收缩期间占主导（峰值速度，15.6±5.8厘米/秒）。异丙肾上腺素使这种正向血流速度的加速率增加了121%（p< 0.01）。硝酸甘油在心房动脉或静脉中未显著改变血流速度波形。心房心肌的动脉流入和静脉流出之间的相位相反表明，由于心房心肌血管容量的存在，流向心房心肌的大部分冠状动脉血流可能被储存。我们得出结论，心房心肌收缩阻碍心房流入并促进心房容量血管的静脉流出。
