Sympathetic stimulation and norepinephrine infusion modulate extracellular potassium concentration during acute myocardial ischemia.
Sympathetic stimulation and norepinephrine infusion modulate extracellular potassium concentration during acute myocardial ischemia.
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交感神经刺激和去甲肾上腺素输注可调节急性心肌缺血期间的细胞外钾浓度。
DOI：
10.1161/01.res.71.5.1078
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发表时间：
1992
影响因子：
20.1
通讯作者：
Zipes,DP
中科院分区：
文献类型：
--
作者：
Warner,MR;Kroeker,TS;Zipes,DP
本研究的目的是探讨交感神经刺激是否调制急性心肌缺血引起的细胞外K+浓度（[K+]o）的上升。在35只α-氯醛糖麻醉的狗中，我们测量了在存在和不存在交感神经刺激或去甲肾上腺素输注的情况下急性心肌缺血期间[K+]o的变化。在18只狗中，完成了一系列4个5分钟的左前降支（LAD）远端闭塞。30分钟的再灌注将每个LAD闭塞分开。将4 ~ 5个K（+）敏感电极插入左室中层心肌，由远端LAD灌注。记录心电图II导联、动脉压和[K+]o，并以恒定的周期长度起搏右心房。第一次、第二次和第四次LAD闭塞在没有交感神经刺激或去甲肾上腺素输注的情况下进行。第一次左前降支闭塞引起的[K+]o变化与第二次和第四次闭塞引起的[K+]o变化不同（p < 0.05）。然而，第二次和第四次LAD闭塞期间[K+]o的变化相似（p > 0.2），并作为第三次闭塞期间获得的反应的对照。在第三次LAD闭塞前2分钟，交感神经刺激（4 Hz）或去甲肾上腺素输注（0.25-0.5 μ g/kg/min i. v.）开始并持续至再灌注后2分钟。我们发现，交感神经刺激和去甲肾上腺素输注增加心肌血流量在正常和缺血组织（P < 0.05）。用23个K（+）敏感电极记录的11条狗的平均反应表明，与第二次和第四次闭塞相比，交感神经刺激在LAD闭塞开始后1、2、3、4和5分钟增加[K+]o（p < 0.001）。与此相反，在7只狗中，20个K（+）敏感电极记录的平均反应表明，在LAD闭塞开始后4和5分钟，去甲肾上腺素输注降低了[K+]o（p < 0.02）。这些数据表明，交感神经刺激增加了急性心肌缺血诱发的[K+]o，这一作用不能通过静脉注射去甲肾上腺素来模拟。
The purpose of this study was to investigate whether sympathetic stimulation modulated the rise in extracellular K+ concentration ([K+]o) evoked by acute myocardial ischemia. In 35 alpha-chloralose-anesthetized dogs, we measured changes in [K+]o during acute myocardial ischemia in the presence and absence of sympathetic stimulation or norepinephrine infusion. A series of four 5-minute occlusions of the distal left anterior descending coronary artery (LAD) was completed in 18 dogs. Thirty minutes of reperfusion separated each LAD occlusion. Four to five K(+)-sensitive electrodes were inserted into the left ventricular midmyocardium that was perfused by the distal LAD. Lead II of the electrocardiogram, arterial pressure, and [K+]o were recorded, and the right atrium was paced at a constant cycle length. The first, second, and fourth LAD occlusions were done in the absence of sympathetic stimulation or norepinephrine infusion. The changes in [K+]o evoked by the first LAD occlusion differed (p < 0.05) from those elicited by the second and fourth occlusions. However, the changes in [K+]o during the second and fourth LAD occlusions were similar (p > 0.2) and served as controls for the responses obtained during the third occlusion. Two minutes before the third LAD occlusion, sympathetic stimulation (4 Hz) or norepinephrine infusion (0.25-0.5 micrograms/kg per minute i.v.) was begun and was continued until 2 minutes after reperfusion. We found that sympathetic stimulation and norepinephrine infusion increased (p < 0.05) myocardial blood flow in both normal and ischemic tissue. The mean response recorded by 23 K(+)-sensitive electrodes in 11 dogs showed that sympathetic stimulation increased (p < 0.001) the [K+]o at 1, 2, 3, 4, and 5 minutes after the onset of LAD occlusion compared with the second and fourth occlusions. In contrast, the mean response recorded by 20 K(+)-sensitive electrodes in seven dogs showed that norepinephrine infusion reduced (p < 0.02) the [K+]o at 4 and 5 minutes after the onset of LAD occlusion. These data show that sympathetic stimulation increased the [K+]o evoked by acute myocardial ischemia, an effect that was not mimicked by the intravenous administration of norepinephrine.