Effects of intracoronary dipyridamole infusion on regional myocardial blood flow and intrinsic thallium-201 washout in dogs with a critical coronary stenosis.
Effects of intracoronary dipyridamole infusion on regional myocardial blood flow and intrinsic thallium-201 washout in dogs with a critical coronary stenosis.
复制标题
冠状动脉内双嘧达莫输注对严重冠状动脉狭窄犬局部心肌血流和内在铊 201 冲洗的影响。
DOI：
10.1016/0002-8703(92)90920-q
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发表时间：
1992
影响因子：
4.8
通讯作者：
Watson,DD
中科院分区：
文献类型：
--
作者：
Beller,GA;Granato,JE;Cannon,JM;Belardinelli,L;Watson,DD
静脉内潘生丁（DP）输注产生一个显着的心内膜到心外膜血流梯度远端的关键冠状动脉狭窄，导致减少区域铊-201（Tl-201）的摄取和洗脱。静脉内DP也可显著降低动脉血压，从而降低冠状动脉灌注压。我们决定采用冠状动脉内DP给药进一步阐明这种透壁冠状动脉“盗血”的机制，从而避免全身性低血压。在8只严重左前降支（LAD）狭窄的犬中，5只冠状动脉内DP未导致体循环动脉压显著下降，心外膜流量从1.15 ± 0.2 ml/min/gm增加至1.75 ± 0.2 ml/min/gm，内膜下流量从1.15 ± 0.2 ml/min/gm轻微下降至1.03 ± 0.5 ml/min/gm。冠状动脉内DP不会延长固有的Tl-201洗脱率。在冠状动脉内DP后发生全身性低血压的3只犬中，心内膜流量从1.14 ml/min/gm降至0.63 ml/min/gm，心外膜/心内膜流量比降至0.35，Tl-201洗脱时间延长。因此，在严重LAD狭窄的情况下，冠状动脉内DP引起最小的心内膜-心外膜盗血，除非伴随全身动脉压下降，否则对固有的Tl-201洗脱率没有影响。透壁盗血的幅度远小于我们以前使用静脉内DP输注的实验中报告的幅度。这项研究提供了一个更深入的了解DP诱导的内膜下缺血的机制，并表明，全身血流动力学的改变发挥了重要作用的影响，血管扩张剂对心肌血流量和TI-201动力学。
Intravenous dipyridamole (DP) infusion produces a significant endocardial-to-epicardial flow gradient distal to a critical coronary stenosis, resulting in diminished regional thallium-201 (Tl-201) uptake and washout. Intravenous DP can also produce a significant decrease in arterial blood pressure and therefore in coronary perfusion pressure. We determined to further clarify the mechanism of this transmural coronary “steal” employing intracoronary DP administration, thereby avoiding systemic hypotension. In five of eight dogs with a critical left anterior descending (LAD) stenosis, intracoronary DP caused no significant fall in systemic arterial pressure, a rise in epicardial flow from 1.15 ± 0.2 to 1.75 ± 0.2 ml/min/gm, and a slight fall in subendocardial flow from 1.15 ± 0.2 to 1.03 ± 0.5 ml/min/gm. Intracoronary DP caused no prolongation of the intrinsic Tl-201 washout rate. In three dogs that developed systemic hypotension after intracoronary DP, endocardial flow fell from 1.14 to 0.63 ml/min/gm, the epicardial/endocardial flow ratio fell to 0.35, and Tl-201 washout became more prolonged. Thus intracoronary DP in the setting of a critical LAD stenosis caused minimal endocardial-to-epicardial steal and had no effect on the intrinsic Tl-201 washout rate unless it was accompanied by a fall in systemic arterial pressure. The magnitude of the transmural steal was substantially less than reported in our previous experiments utilizing intravenous DP infusion. This study provides a further insight into the mechanism of DP-induced subendocardial ischemia and suggests that systemic hemodynamic alterations play an important role in the effects of the vasodilator on myocardial blood flow and Tl-201 kinetics.