Kanatsuka H, Lamping K G, Eastham C L, Dellsperger K C, Marcus M L
Department of Internal Medicine, University of Iowa, College of Medicine, Iowa City 52242.
Circ Res. 1989 Nov;65(5):1296-305. doi: 10.1161/01.res.65.5.1296.
The purposes of this study were to determine if coronary dilation secondary to an increase in myocardial oxygen consumption (MVO2) affects the microcirculation in a homogeneous or heterogeneous manner and to determine if comparable degrees of coronary dilation produced by increasing MVO2 or exogenous (intravenous adenosine) or endogenous (intravenous dipyridamole) adenosine have similar effects in the coronary microcirculation. The epimyocardial coronary microcirculation was observed through an intravital microscope by stroboscopic epi-illumination in anesthetized open-chest dogs. Aortic pressure and heart rate were controlled by an aortic snare and atrioventricular sequential pacing, respectively, during experimental procedures. In group 1 (n = 15), coronary arterial microvessel diameters were measured under control condition and during rapid pacing at 300 beats/min, which doubled MVO2. Increases in MVO2 caused heterogeneous vasodilation in coronary arterial microvessels (40-380 microns). There was an inverse relation between control diameter and percent increase in diameter. In group 2 (n = 15) or group 3 (n = 10), adenosine or dipyridamole was infused intravenously to increase myocardial perfusion to the same level as that obtained with rapid pacing. Adenosine and dipyridamole did not change MVO2. Adenosine and dipyridamole also caused heterogeneous vasodilation, but the effects of adenosine and dipyridamole were restricted to arterial microvessels smaller than 150 microns. From these results, we conclude that increases in MVO2 produce widespread but heterogeneous vasodilation, that is, greater dilation in smaller arterial microvessels. Comparable increases in coronary flow produced by increasing MVO2 or endogenous and exogenous adenosine do not produce identical changes in the distribution of coronary microvascular resistance.
本研究的目的是确定继发于心肌耗氧量（MVO2）增加的冠状动脉扩张是以均匀或非均匀方式影响微循环，以及确定通过增加MVO2或外源性（静脉注射腺苷）或内源性（静脉注射双嘧达莫）腺苷产生的同等程度的冠状动脉扩张在冠状动脉微循环中是否具有相似作用。在麻醉开胸犬中，通过频闪落射照明利用活体显微镜观察心外膜冠状动脉微循环。在实验过程中，分别通过主动脉圈套器和房室顺序起搏控制主动脉压和心率。在第1组（n = 15）中，在对照条件下以及在300次/分钟的快速起搏期间测量冠状动脉微血管直径，快速起搏使MVO2增加一倍。MVO2增加导致冠状动脉微血管（40 - 380微米）出现非均匀性血管扩张。对照直径与直径增加百分比之间呈负相关。在第2组（n = 15）或第3组（n = 10）中，静脉注射腺苷或双嘧达莫以将心肌灌注增加至与快速起搏时相同的水平。腺苷和双嘧达莫未改变MVO2。腺苷和双嘧达莫也导致非均匀性血管扩张，但腺苷和双嘧达莫的作用仅限于直径小于150微米的动脉微血管。从这些结果中，我们得出结论，MVO2增加会产生广泛但非均匀的血管扩张，即在较小的动脉微血管中扩张更大。通过增加MVO2或内源性和外源性腺苷产生的冠状动脉血流的同等增加不会在冠状动脉微血管阻力分布上产生相同的变化。
