Protection Against Autonomic Denervation Following Acute Myocardial Infarction by Preconditioning Ischemia
Protection Against Autonomic Denervation Following Acute Myocardial Infarction by Preconditioning Ischemia
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通过预处理缺血来防止急性心肌梗死后的自主神经失控
DOI：
10.1161/01.res.64.3.437
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发表时间：
1989
影响因子：
20.1
通讯作者：
D. Zipes
中科院分区：
文献类型：
--
作者：
Toshihisa Miyazaki;D. Zipes
为探讨缺血预适应对急性跨壁心肌缺血/梗死(MI)后传出自主神经反应的影响，比较了接受一期持续性冠脉阻断的对照组和4只冠脉阻断后再灌注5min再灌流5min的预适应犬传出交感神经和迷走神经支配的时程和程度。结扎冠状动脉左前降支斜角支，分别于缺血前、阻断后及持续阻断后20、60、120、180min，在基础状态、神经刺激时测定心肌梗死基础和心尖部有效不应期(ERP)。在10只跨壁MI的对照犬中，刺激双侧锁骨下动脉4毫秒脉冲(2-4 Hz和2-4 mA)引起的ERP缩短在基础部位没有变化，但在心尖部位减弱。持续闭塞20分钟后，40个心尖试验点中有4个出现传出交感神经支配(缩短±2毫秒)。在3个小时内，40个根尖部位中有13个失去了神经。在10只预适应犬中，在预适应闭塞后和持续缺血的前60分钟，心尖部位的ERP缩短没有变化，但在120分钟时减弱。40个心尖试验点中有3个在3小时内失去了神经。尽管心外膜下受累程度相当(8.2±1.0%；vs.8.4±1.4%；与左心室周长之比，均值±扫描电子显微镜)，预适应组失神经心尖试验部位的累积百分比明显低于对照组(p=0.006)。在11只接受MI后迷走神经传出反应测试的对照犬中，双侧迷走神经刺激(4毫秒脉冲，20赫兹，电流强度比产生停搏所需的电流强度大0.05 mA)诱发的ERP延长在基础部位没有变化，但在心尖部位减弱，44个试验点中有5个在持续冠脉阻断20分钟后出现失神经(±1毫秒延长)。在3个小时内，40个根尖部位中有14个失去了神经。在10只预适应犬中，迷走神经诱发的事件相关电位延长在基础和心尖部位都没有变化，36个心尖部位在预适应后和持续冠脉闭塞3小时内没有出现失神经支配(P<；0.001比对照组)，尽管心内膜下心肌梗死的受累程度相当(11.8±0.8%比11.9±1.3%)。在预适应心脏中，放射性微球测量的缺血心肌在持续冠脉阻断期间的血流减少与第一次预适应阻断时相似，表明MI期间侧支血流的增加不能解释预适应的保护作用。我们的结论是，短暂的缺血预适应在犬冠状动脉闭塞后的早期保留了传出交感神经和迷走神经的反应，其机制尚不确定。
To examine the effects of ischemic preconditioning on efferent autonomic responses following acute transmural myocardial ischemia/infarction (MI), the time course and extent of efferent sympathetic and vagal denervation were compared between control dogs that received a one-stage sustained coronary occlusion and preconditioned dogs that received four 5-minute coronary occlusions separated by 5 minutes of reperfusion before sustained occlusion. Effective refractory periods (ERP) basal and apical to MI were determined in the baseline state and during neural stimulation before and after preconditioning occlusions and 20, 60, 120, and 180 minutes after sustained occlusion by ligature ligation of diagonal branches of the left anterior descending coronary artery. In 10 control dogs with transmural MI, ERP shortening induced by bilateral ansae subclaviae stimulation (4-msec pulses, 2-4 Hz and 2-4 mA) was unchanged at basal sites but was attenuated at apical sites. Four of 40 apical test sites exhibited efferent sympathetic denervation (±2 msec shortening) 20 minutes after sustained occlusion. Thirteen of 40 apical sites became denervated during a 3-hour period. In 10 preconditioned dogs, ERP shortening at apical sites was unchanged after preconditioning occlusions and during the first 60 minutes of sustained ischemia but was attenuated at 120 minutes. Three of 40 apical test sites became denervated during a 3-hour period. The cumulative percentage of denervated apical test sites was significantly less in the preconditioned group compared with the control group (p=0.006) despite a comparable degree of subepicardial involvement in the MI (8.2±1.0percent; vs. 8.4±1.4percent;, the ratio to the left ventricular circumference, mean±SEM). In 11 control dogs tested for efferent vagal response after MI, ERP prolongation induced by bilateral vagal stimulation (4-msec pulses, 20 Hz with current strength 0.05 mA greater than that required to produce asystole) was unchanged at basal sites, but was attenuated at apical sites, and five of 44 test sites exhibited denervation (±1 msec prolongation) 20 minutes after sustained coronary occlusion. Fourteen of 40 apical sites became denervated during a 3-hour period. In 10 preconditioned dogs, vagally induced ERP prolongation was unchanged both at basal and apical sites, and none of 36 apical test sites exhibited denervation after preconditioning and during a 3-hour period of sustained coronary occlusion (p<0.001 vs. control group) despite a comparable degree of subendocardial involvement in the MI (11.8±0.8percent; vs. 11.9±1.3percent;). In preconditioned hearts, the blood flow reduction to the ischemic myocardium measured by radioactive microspheres during sustained coronary occlusion was comparable with that during the first preconditioning occlusion, indicating that an increase in collateral blood flow during MI cannot explain the protective effects of preconditioning. We conclude that preconditioning with brief episodes of ischemia preserves efferent sympathetic and vagal responses during the early period after coronary artery occlusion in the dog by mechanisms still to be determined.
影响因子：
--
作者：
TAKAHASHI, N;BARBER, MJ;ZIPES, DP
通讯作者：
ZIPES, DP
重复发生短暂缺血（12 分钟）不会累积消耗高能磷酸盐化合物。
影响因子：
10.8
作者：
Swain,JL;Sabina,RL;Hines,JJ;GreenfieldJr,JC;Holmes,EW
通讯作者：
Holmes,EW