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狭窄在体内对心内膜下和心外膜下小动脉的影响不同。

Stenosis differentially affects subendocardial and subepicardial arterioles in vivo.

作者信息

Merkus D, Vergroesen I, Hiramatsu O, Tachibana H, Nakamoto H, Toyota E, Goto M, Ogasawara Y, Spaan J A, Kajiya F

机构信息

Department of Medical Physics, Cardiovascular Research Institute Amsterdam, Academic Medical Center, University of Amsterdam, 1100 DE Amsterdam, The Netherlands.

出版信息

Am J Physiol Heart Circ Physiol. 2001 Apr;280(4):H1674-82. doi: 10.1152/ajpheart.2001.280.4.H1674.

DOI:10.1152/ajpheart.2001.280.4.H1674
PMID:11247779
Abstract

The presence of a coronary stenosis results primarily in subendocardial ischemia. Apart from the decrease in coronary perfusion pressure, a stenosis also decreases coronary flow pulsations. Applying a coronary perfusion system, we compared the autoregulatory response of subendocardial (n = 10) and subepicardial (n = 12) arterioles (<120 microm) after stepwise decreases in coronary arterial pressure from 100 to 70, 50, and 30 mmHg in vivo in dogs (n = 9). Pressure steps were performed with and without stenosis on the perfusion line. Maximal arteriolar diameter during the cardiac cycle was determined and normalized to its value at 100 mmHg. The initial decrease in diameter during reductions in pressure was significantly larger at the subendocardium. Diameters of subendocardial and subepicardial arterioles were similar 10--15 s after the decrease in pressure without stenosis. However, stenosis decreased the dilatory response of the subendocardial arterioles significantly. This decreased dilatory response was also evidenced by a lower coronary inflow at similar average pressure in the presence of a stenosis. Inhibition of nitric oxide production with N(G)-monomethyl-L-arginine abrogated the effect of the stenosis on flow. We conclude that the decrease in pressure caused by a stenosis in vivo results in a larger decrease in diameter of the subendocardial arterioles than in the subepicardial arterioles, and furthermore stenosis selectively decreases the dilatory response of subendocardial arterioles. These two findings expand our understanding of subendocardial vulnerability to ischemia.

摘要

冠状动脉狭窄主要导致心内膜下缺血。除了冠状动脉灌注压降低外,狭窄还会减少冠状动脉血流搏动。应用冠状动脉灌注系统,我们在犬体内(n = 9)将冠状动脉压力从100 mmHg逐步降至70、50和30 mmHg后,比较了心内膜下(n = 10)和心外膜下(n = 12)小动脉(<120微米)的自动调节反应。在灌注线上有或无狭窄的情况下进行压力阶跃。确定心动周期中的最大小动脉直径,并将其标准化为100 mmHg时的值。在心内膜下,压力降低期间直径的初始减小明显更大。在无狭窄的压力降低后10 - 15秒,心内膜下和心外膜下小动脉的直径相似。然而,狭窄显著降低了心内膜下小动脉的扩张反应。在存在狭窄的情况下,类似平均压力下较低的冠状动脉流入量也证明了这种降低的扩张反应。用N(G)-单甲基-L-精氨酸抑制一氧化氮生成消除了狭窄对血流的影响。我们得出结论,体内狭窄引起的压力降低导致心内膜下小动脉直径的减小比心外膜下小动脉更大,而且狭窄选择性地降低了心内膜下小动脉的扩张反应。这两个发现扩展了我们对心内膜下缺血易感性的理解。

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