Simulated ischemia does not protect against efferent sympathetic denervation following acute myocardial infarction in canine hearts.
Simulated ischemia does not protect against efferent sympathetic denervation following acute myocardial infarction in canine hearts.
复制标题
模拟缺血不能防止犬心脏急性心肌梗塞后传出交感神经去神经支配。
DOI：
10.1111/j.1540-8167.1993.tb01209.x
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发表时间：
1993
影响因子：
2.7
通讯作者：
Zipes,DP
中科院分区：
文献类型：
--
作者：
Rubart,M;Pride,HP;Kroeker,TS;Warner,MR;Zipes,DP
缺血期间模拟预处理对神经反应的影响：简介：短暂缺血预处理心肌可通过尚不清楚的机制保护非梗死心肌顶端对急性透壁缺血部位的传出自主反应。我们假设心肌反复短暂暴露于模拟的缺血环境，包括缺氧、高钾。方法和结果：开胸麻醉的狗在左颈动脉和左前降支的对角分支之间接受额外的冠状动脉旁路。我们分析了模拟缺血对三组犬在随后3小时持续缺血期间传出交感神经去神经支配的时间过程和程度的影响：两组犬接受了4个周期的5分钟冠状动脉内灌注，其中一个周期是低氧改变的台氏液，（12 mM K+，6.8 pH和10 μ腺苷; n = 11）或正常台氏液（1 ml）。每次台氏灌注通过5分钟的血液灌注分开，然后通过环形冠状动脉的乳胶再动员进行永久性冠状动脉闭塞。第三组在最终缺血发作前接受连续3小时血液灌注（n = 5）。在灌注前和灌注后以及持续闭塞后20、60、120和180分钟，测定双侧鞍下袢刺激（2 - 4 Hz）基底和心尖至干预部位诱导的有效不应期（ERP）缩短。在所有组中，交感神经诱导的ERP缩短在整个实验过程中在基底部位没有变化。在用改变的或正常的台氏液灌注后或在连续3小时血液灌注后，心尖部位的ERP缩短没有变化。然而，在所有组中，冠状动脉闭塞后心尖部位的EKP缩短显著减弱。在3小时永久性缺血期间，两组间心尖测试部位交感神经诱导的ERP缩短的减少量和去神经心尖测试部位（缩短≤ 2 msec）的累积百分比均无显著差异（分别为P = 0.052和P = 0.752）。心外膜下参与心肌梗死的程度在各组之间具有可比性。结论：因此，在随后的永久性冠状动脉闭塞之前，左心室心肌短暂暴露于缺血代谢物不会触发负责保护跨壁心肌梗死/缺血区域顶端传出交感神经去神经支配的机制。
Effect of Simulated Preconditioning on Neural Response During Ischemia.Introduction:Preconditioning the myocardium with brief episodes of ischemia preserves efferent autonomic responsiveness of noninfarcted myocardium apical to a site of acute transmural ischemia by mechanism(s) still unknown. We hypothesized that repeated brief exposure of the myocardium to a simulated ischemic milieu including hypoxia, high K. low pH, and adenosine would be as effective as brief coronary occlusions in creating this protection.Methods and Results:Open chest anesthetized dogs received an extra corporeal bypass between the left carotid artery and a diagonal branch of the left anterior descending coronary artery. We analyzed the effects of simulated ischemia on the time course and extent of efferent sympathetic denervation during a subsequent 3‐hour sustained ischemia in three groups of dogs: two groups of dogs underwent four cycles of 5‐minute intracoronary perfusion with either hypoxic altered Tyrode's solution (12 mM K+, 6.8 pH, and 10 μ adenosine; n = 11) or normal Tyrode's solution mil. Each Tyrode's perfusion was separated by 5 minutes of blood perfusion prior to permanent coronary occlusion by latex remobilization of the annulated coronary artery. A third group received a continuous 3‐hour blood perfusion before the final ischemic episode (n = 5). Shortening of effective refractory periods (ERPs) induced by bilateral ansae subelaviae stimulation (2 to 4 Hz) basal and apical to the intervention site was determined before and after perfusions and 20, 60, 120, and 180 minutes after sustained occlusion. In all groups, sympathetically‐induced ERP shortening was unchanged at basal sites throughout the experiment. ERP shortening at apical sites was unchanged after perfusions with either the altered or normal Tyrode's solution or after a continuous 3‐hour blood perfusion. However, EKP shortening became significantly attenuated at apical sites after coronary occlusion in all groups. Neither the size in reduction of sympathetically‐induced ERP shortening at apical test sites nor the cumulative percentage of denervated apical test sites (≤ 2‐msec shortening) during a 3‐hour period of permanent ischemia differed significantly among groups (P = 0.052 and P = 0.752, respectively). The degree of subepicardial involvement in the myocardial infarction was comparable among groups.Conclusion:Thus, brief exposure of the left ventricular myocardium to ischemic metabolites prior to a subsequent permanent coronary occlusion does not trigger mechanism(s) that are responsible for protection against efferent sympathetic denervation apical to an area of trans‐mural myocardial infarction/ischemia.