Mirvis D M, Ramanathan K B, Wilson J L
Medical Service, Memphis Veterans Administration Medical Center, TN.
Am Heart J. 1988 May;115(5):984-92. doi: 10.1016/0002-8703(88)90067-1.
Altering regional myocardial flow by the use of potent vasodilators as well as increasing oxygen demand by exercise have been employed as diagnostic methods for detecting coronary arterial obstruction. We sought to define the relative capabilities of these two methods to produce abnormal ECG patterns and to alter myocardial blood flow after Ameroid constriction of the left circumflex coronary artery. Atrial pacing to rates of 210 beats/min was performed, followed by intravenous administration of 0.25 and 0.50 mg/kg of dipyridamole. ECGs were recorded to construct body surface isopotential distributions. Flow was measured by serial injections of radiolabelled microspheres. In 15 animals studied after 3 to 5 weeks of Ameroid constriction, pacing increased epicardial flow by 19.14 +/- 7.11% but reduced endocardial flow by 35.69 +/- 12.32%, with a significant reduction (to less than 0.67) in the endocardial/epicardial flow ratio in 12 (80%) dogs; both endocardial and epicardial flows were significantly lower in the ischemic than in the nonischemic bed. Ten dogs developed abnormal ST segment responses of subendocardial ischemia. In contrast, dipyridamole produced a dose-dependent rise in both endocardial (25.33 +/- 8.54% and 55.80 +/- 9.22% after 0.25 and 0.5 mg/kg, respectively) and epicardial (29.13 +/- 7.49% and 66.33 +/- 7.64% after 0.25 and 0.5 mg/kg, respectively) flows without a significant fall in the transmural ratio. These increases were, however, significantly less than those observed in nonischemic bed flow, resulting in a transventricular gradient of blood flow. No dog developed abnormal ECG patterns after dipyridamole infusion. Thus pacing produces both a transmural and a transventricular gradient in blood flow, whereas vasodilation causes only a transventricular flow abnormality.(ABSTRACT TRUNCATED AT 250 WORDS)
通过使用强效血管扩张剂改变局部心肌血流以及通过运动增加氧需求,已被用作检测冠状动脉阻塞的诊断方法。我们试图确定这两种方法在左旋冠状动脉Ameroid缩窄后产生异常心电图模式和改变心肌血流的相对能力。以210次/分钟的速率进行心房起搏,随后静脉注射0.25和0.50mg/kg的双嘧达莫。记录心电图以构建体表等电位分布。通过连续注射放射性标记的微球来测量血流。在Ameroid缩窄3至5周后研究的15只动物中,起搏使心外膜血流增加19.14±7.11%,但使心内膜血流减少35.69±12.32%,12只(80%)犬的心内膜/心外膜血流比值显著降低(降至小于0.67);缺血床的内膜和外膜血流均显著低于非缺血床。10只犬出现心内膜下缺血的异常ST段反应。相比之下,双嘧达莫使心内膜(分别在0.25和0.5mg/kg后为25.33±8.54%和55.80±9.22%)和心外膜(分别在0.25和0.5mg/kg后为29.13±7.49%和66.33±7.64%)血流呈剂量依赖性增加,而跨壁比值无显著下降。然而,这些增加显著低于非缺血床血流中观察到的增加,导致跨心室血流梯度。双嘧达莫输注后没有犬出现异常心电图模式。因此,起搏会产生跨壁和跨心室的血流梯度,而血管扩张仅导致跨心室血流异常。(摘要截短于250字)