Picano E, Lattanzi F, Distante A, L'Abbate A
C.N.R. Institute of Clinical Physiology, Pisa, Italy.
Am Heart J. 1989 Aug;118(2):314-9. doi: 10.1016/0002-8703(89)90191-9.
The aim of this study was to assess whether myocardial oxygen consumption can be responsible for aminophylline resistance in dipyridamole-induced ischemia. We analyzed 163 consecutive patients who had a positive low-dose (0.56 mg/kg over 4 minutes) dipyridamole-echocardiography test, requiring intravenous aminophylline as an antidote. All patients also performed an exercise stress test. In 141 of these patients, the signs of ischemia were reversed by administration of intravenous aminophylline (group I), while the remaining 22 patients were resistant to aminophylline (240 mg/kg over 3 minutes) and received additional treatment with nitrates to relieve ischemia (group II). The increase in rate-pressure product (RPP = mm Hg x beats/min x 100) measured during the exercise stress test in the patients in group I was significantly greater than that determined during dipyridamole-induced ischemia (204 +/- 41 versus 145 +/- 33, p less than 0.01). However, the increases in RPP under both conditions were similar for the patients in group II (147 +/- 24 versus 150 +/- 20, p = ns). In patients with dipyridamole-induced ischemia who were resistant to aminophylline, the rise in myocardial oxygen consumption--probably linked to reflex sympathetic activation--might maintain ischemia independently from flow maldistribution, which should be reversed by aminophylline.
本研究的目的是评估心肌耗氧量是否可导致双嘧达莫诱发缺血时对氨茶碱产生抵抗。我们分析了163例连续的患者，这些患者低剂量（4分钟内0.56mg/kg）双嘧达莫超声心动图试验呈阳性，需要静脉注射氨茶碱作为解毒剂。所有患者还进行了运动负荷试验。在这些患者中，141例患者静脉注射氨茶碱后缺血体征得到逆转（I组），而其余22例患者对氨茶碱（3分钟内240mg/kg）耐药，接受了硝酸盐额外治疗以缓解缺血（II组）。I组患者运动负荷试验期间测得的心率-血压乘积（RPP = mmHg×心率/分钟×100）增加显著大于双嘧达莫诱发缺血期间测定的值（204±41对145±33，p<0.01）。然而，II组患者在两种情况下RPP的增加相似（147±24对150±20，p=无显著性差异）。在双嘧达莫诱发缺血且对氨茶碱耐药的患者中，心肌耗氧量的增加——可能与反射性交感神经激活有关——可能独立于血流分布不均维持缺血，而氨茶碱应可逆转血流分布不均。
