Vagal Stimulation, Through its Nicotinic Action, Limits Infarct Size and the Inflammatory Response to Myocardial Ischemia and Reperfusion
Vagal Stimulation, Through its Nicotinic Action, Limits Infarct Size and the Inflammatory Response to Myocardial Ischemia and Reperfusion
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DOI：
10.1097/fjc.0b013e31822b7204
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发表时间：
2011-11-01
影响因子：
3
通讯作者：
Schwartz, Peter J.
中科院分区：
文献类型：
--
作者：
Calvillo, Laura;Vanoli, Emilio;Schwartz, Peter J.
迷走神经活动对缺血性心脏病具有保护作用。我们测试了迷走神经刺激（VS）是否可以调节炎症反应，炎症反应是缺血/再灌注后心脏损伤的主要决定因素。四组雄性大鼠接受心肌缺血（30 分钟）和再灌注（24 小时）。一组接受 VS（40 分钟）、1 次 VS 加心房起搏（VS + 起搏）、1 次 VS 加美加明烟碱抑制（VS + MEC）。 24小时后，对危险区域、梗塞面积、炎症参数和细胞凋亡进行量化。所有 VS 治疗大鼠的梗塞面积均减少（对照组，53 +/- 18%；VS，6.5 +/- 3%；VS + 起搏，23 +/- 6%；VS + MEC，33 +/- 9%；与对照组相比，P < 0.005）。尽管心率相似，VS + MEC 组的梗死面积仍大于 VS 治疗组的梗死面积，表明部分保护丧失。在所有接受 VS 治疗的动物中，危险区域中巨噬细胞、中性粒细胞和凋亡细胞的数量以及血浆细胞因子水平均显着降低。总之，VS 可减少缺血/再灌注期间的梗塞面积和炎症标志物，与心率无关。烟碱途径的抗炎和抗凋亡特性是主要的潜在机制。迷走神经介导的炎症反应调节可能在急性冠脉综合征和心力衰竭的临床治疗中有价值。
Vagal activity has protective effects in ischemic heart disease. We tested whether vagal stimulation (VS) could modulate the inflammatory reaction, a major determinant of cardiac injury after ischemia/reperfusion. Four groups of male rats underwent myocardial ischemia (30 minutes) and reperfusion (24 hours). One group underwent VS (40 minutes), 1 VS plus atrial pacing (VS + Pacing), and 1 VS plus nicotinic inhibition by mecamylamine (VS + MEC). After 24 hours, the area at risk, infarct size, inflammation parameters, and apoptosis were quantified. Infarct size was reduced in all VS-treated rats (controls, 53 +/- 18%; VS, 6.5 +/- 3%; VS + Pacing, 23 +/- 6%; VS + MEC, 33 +/- 9%; P < 0.005 vs. controls). The infarct size in the VS + MEC group was larger than that in VS-treated animals, despite similar heart rate, suggesting partial loss of protection. The number of macrophages, neutrophils, and apoptotic cells in the area at risk and the plasma cytokines levels were significantly reduced in all VS-treated animals. In conclusion, VS decreases infarct size and inflammatory markers during ischemia/reperfusion independent of the heart rate. The anti-inflammatory and antiapoptotic properties of the nicotinic pathway are the primary underlying mechanism. The vagally mediated modulation of inflammatory responses may prove valuable in the clinical management of acute coronary syndromes and of heart failure.