Effects of cocaine on cardiac vagal tone before and during coronary artery occlusion: cocaine exacerbates the autonomic response to myocardial ischemia.
Effects of cocaine on cardiac vagal tone before and during coronary artery occlusion: cocaine exacerbates the autonomic response to myocardial ischemia.
复制标题
可卡因对冠状动脉闭塞之前和期间心脏迷走神经张力的影响：可卡因加剧对心肌缺血的自主反应。
DOI：
10.1097/00005344-199312000-00015
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发表时间：
1993
影响因子：
3
通讯作者：
Lappi,MD
中科院分区：
文献类型：
--
作者：
Billman,GE;Lappi,MD
可卡因是一种强效拟交感神经药物，可引发致命的心脏事件。可卡因引起的自主平衡改变，特别是在心肌缺血期间，可能会显着导致这些不良反应。为了检验这一假设，我们对未麻醉的杂种狗（n = 7）进行了 2 分钟的左回旋冠状动脉（LCX）闭塞，用仪器测量左心室压力（LVP）、心室电图和冠状动脉血流（CBF），有或没有不同剂量的可卡因（0.0、0.5、1、2 和 4 mg/kg）。可卡因剂量之间至少相隔 24 小时，剂量是随机的。心率（HR）变异性的时间序列分析被用作心脏迷走神经张力（0.24-1.04 Hz）的指标。可卡因会引起心率的剂量依赖性增加，同时伴随着心脏迷走神经张力的相应降低。给予可卡因约 1 分钟后达到峰值反应，并在 15 分钟（0.5 和 1 毫克/千克）、30 分钟（2 毫克/千克）或 60 分钟（4 毫克/千克）后恢复到前可卡因值。心肌缺血导致 HR 显着增加，心脏迷走神经张力降低，可卡因（1、2 和 4 mg/kg）会加剧这种情况；例如，可卡因 (2 mg/kg) 引起更大的 HR（对照 119.3+/-5.9，闭塞 149.7+/-9.6；可卡因 144+/-11.9，闭塞 178.3+/-10.4 次/分钟）和迷走神经张力（对照 5.6+/-0.7，闭塞 2.6+/-0.3；可卡因 5.2+/-0.7，闭塞1.3+/-0.5 在s2)中对2分钟冠状动脉闭塞的反应。β-肾上腺素受体阻滞(盐酸普萘洛尔1mg/kg)减弱了HR反应，但在冠状动脉闭塞期间引起迷走神经张力的更大降低(达到较低值)。这些数据表明，可卡因不仅会引起肾上腺素能活性的增加，还会降低心脏迷走神经张力。特别是，可卡因会加剧对心肌缺血的自主反应。由此产生的自主神经失衡可能会增加恶性心律失常的倾向
Cocaine is a potent sympathomimetic drug that can provoke lethal cardiac events. Cocaine-induced alterations in autonomic balance, particularly during myocardial ischemia, could contribute significantly to these adverse reactions. To test this hypothesis, we produced a 2-min left circumflex coronary artery (LCX) occlusion in unanesthetized mongrel dogs (n= 7) instrumented to measure left ventricular pressure (LVP), ventricular electrogram, and coronary blood flow (CBF) with and without various doses of cocaine (0.0, 0.5, 1, 2, and 4 mg/kg). At least 24 h elapsed between cocaine doses, which were given in random order. Time series analysis of heart rate (HR) variability was used as an index of cardiac vagal tone (0.24-1.04 Hz). Cocaine elicited dosedependent increases in HR that were accompanied by corresponding decreases in cardiac vagal tone. The peak response was achieved~ 1 min after cocaine was given and returned to precocaine values 15 (0.5 and 1 mg/kg), 30 (2 mg/kg), or 60 (4 mg/kg) min later. Myocardial ischemia elicited significant increases in HR and reductions in cardiac vagal tone that were accentuated by cocaine (1, 2, and 4 mg/kg); eg, cocaine (2 mg/kg) elicited a greater HR (control 119.3+/-5.9, occlusion 149.7+/-9.6; cocaine 144+/-11.9, occlusion 178.3+/-10.4 beats/min) and vagal tone (control 5.6+/-0.7, occlusion 2.6+/-0.3; cocaine 5.2+/-0.7, occlusion 1.3+/-0.5 In s2) response to 2-min coronary occlusion.[beta]-Adrenoceptor blockade (propranolol HCl 1 mg/kg) attenuated the HR response but elicited greater reduction (lower values were achieved) in vagal tone during coronary artery occlusion. These data demonstrate that cocaine not only provokes an increase in adrenergic activity but also reduces cardiac vagal tone. In particular, cocaine exacerbates the autonomic response to myocardial ischemia. The resulting autonomic imbalance could increase the propensity for malignant arrhythmias