Canty J M, Klocke F J
Circulation. 1985 Feb;71(2):370-7. doi: 10.1161/01.cir.71.2.370.
To determine whether reductions in regional myocardial perfusion at reduced coronary arterial pressures reliably indicate maximal vasodilation of the distal vasculature, coronary autoregulation was studied in open-chest dogs at heart rates of approximately 60 beats/min, a level at which metabolic demand, time-averaged systolic compressive forces, and transmural vasodilator reserve approximate those found under usual resting conditions. Circumflex pressure was controlled with a programmable pressure source. Regional circumflex inflow was 0.56 +/- 0.04(SEM) ml . min-1 . g-1 when circumflex pressure equaled spontaneous aortic pressure and fell to 0.34 +/- 0.02 ml . min-1 . g-1 when circumflex pressure was reduced to 35 mm Hg. Reductions were similar in each myocardial layer, with endocardial flow falling from 0.68 +/- 0.04 to 0.39 +/- 0.03 ml . min-1 . g-1. During adenosine-induced vasodilation at 35 mm Hg, full-thickness and endocardial flows rose to 0.92 +/- 0.08 and 1.07 +/- 0.10 ml . min-1 . g-1, respectively. When coronary pressure was reduced to 25 mm Hg and autoregulation was again operative, full-thickness and endocardial flows fell to 0.28 +/- 0.03 and 0.28 +/- 0.04 ml . min-1 . g-1. During adenosine vasodilation at 25 mm Hg endocardial flow did not increase significantly but epicardial reserve remained present. These results indicate that significant reductions in regional myocardial perfusion can occur before pharmacologic vasodilator reserve is exhausted. In the absence of tachycardia, endocardial vasodilator reserve can persist to coronary pressures less than 35 mm Hg, but is ordinarily exhausted before epicardial vasodilator reserve.
为了确定在冠状动脉压力降低时局部心肌灌注的减少是否能可靠地表明远端血管床的最大血管舒张，在开胸犬中研究了冠状动脉自动调节，心率约为60次/分钟，在此水平下，代谢需求、时间平均收缩压缩力和跨壁血管舒张储备近似于通常静息状态下的值。用可编程压力源控制回旋支压力。当回旋支压力等于自发主动脉压力时，回旋支局部血流量为0.56±0.04（SEM）ml·min⁻¹·g⁻¹，当回旋支压力降至35mmHg时，血流量降至0.34±0.02ml·min⁻¹·g⁻¹。各心肌层的减少情况相似，心内膜血流量从0.68±0.04降至0.39±0.03ml·min⁻¹·g⁻¹。在35mmHg腺苷诱导的血管舒张过程中，全层和心内膜血流量分别升至0.92±0.08和1.07±0.10ml·min⁻¹·g⁻¹。当冠状动脉压力降至25mmHg且自动调节再次起作用时，全层和心内膜血流量降至0.28±0.03和0.28±0.04ml·min⁻¹·g⁻¹。在25mmHg腺苷血管舒张过程中，心内膜血流量没有显著增加，但心外膜储备仍然存在。这些结果表明，在药理血管舒张储备耗尽之前，局部心肌灌注可能会显著减少。在没有心动过速的情况下，心内膜血管舒张储备可持续到冠状动脉压力低于35mmHg，但通常在心外膜血管舒张储备之前耗尽。
