Department of Anesthesiology and Intensive Care Medicine, Aarhus University Hospital, Denmark.
Acta Anaesthesiol Scand. 2012 Jan;56(1):48-56. doi: 10.1111/j.1399-6576.2011.02577.x. Epub 2011 Nov 21.
Postconditioning (postcon) reduces infarct size, myocardial superoxide ((•)O(2)) generation, and neutrophil (PMN) accumulation. It is unknown whether inhibition of PMNs influence cardioprotection by postcon. The present study tested the following hypotheses: (1) myocardial salvage by postcon is modified by inhibition of PMNs and (2) postcon directly inhibits PMN (•)O(2) generation.
For hypothesis 1, a deductive approach was used to determine infarct size in vivo with and without PMNs in rats, and for hypothesis 2, blood sampled from the anterior interventricular vein (AIV) in a canine model was used. Protocol 1: anesthetized rats, subjected to 30 min of coronary artery occlusion and 3 h of reperfusion, were randomized to control (n = 13), postcon (n = 13), PMN-depletion: (n = 9), and postcon in PMN-depleted rats (n = 9). Protocol 2: blood was sampled at baseline, 2 h and 24 h from the AIV, draining the area at risk (AAR) in anesthetized dogs with 60 min coronary occlusion ± postcon; whole blood was analyzed for (•)O(2) by luminol-enhanced chemiluminescence.
Postcon and PMN depletion reduced infarct size (42.6 ± 2.1%, P < 0.05 vs. control, and 43.9 ± 3.0%, P < 0.05 vs. control, respectively) vs. control (58.8 ± 0.9%), with no further decrease with postcon in PMN-depleted rats (37.2 ± 2.9%, P = 0.34 vs. postcon). PMN accumulation in AAR was less in postcon (21.2 ± 0.3%, P < 0.05 vs. control) and PMN-depleted (9.4 ± 0.3%, P < 0.05 vs. control) vs. control (30.5 ± 1.2%), with a further decrease in the postcon + PMN depletion group (5.4 ± 0.6%, P < 0.05 vs. control). In dogs, (•)O(2) release by PMNs increased at 2 h and 24 h of R, which was reduced to baseline levels by postcon.
These data imply PMN involvement in cardioprotection by postconditioning.
后处理（postcon）可减少梗死面积、心肌超氧化物（（•）O2）的产生和中性粒细胞（PMN）的聚集。目前尚不清楚PMN的抑制是否会影响后处理的心脏保护作用。本研究检验了以下假设：（1）PMN 抑制后处理对心肌挽救的影响；（2）后处理直接抑制 PMN 的（•）O2 的产生。
为了验证假设 1，我们在大鼠体内采用演绎法确定有无 PMN 存在时的梗死面积，为了验证假设 2，我们采用犬模型从前降支静脉（AIV）取样。方案 1：麻醉大鼠，进行 30 分钟的冠状动脉闭塞和 3 小时的再灌注，随机分为对照组（n = 13）、后处理组（n = 13）、PMN 耗竭组（n = 9）和后处理加 PMN 耗竭组（n = 9）。方案 2：在麻醉犬中进行 60 分钟的冠状动脉闭塞加后处理，从 AIV 取样，分析基线、2 小时和 24 小时的血液（•）O2 通过发光增强化学发光法。
后处理和 PMN 耗竭均可降低梗死面积（42.6 ± 2.1%，P < 0.05 与对照组相比，和 43.9 ± 3.0%，P < 0.05 与对照组相比）与对照组（58.8 ± 0.9%）相比，PMN 耗竭后再处理组（37.2 ± 2.9%，P = 0.34 与后处理组相比）无进一步降低。AAR 中 PMN 的积累在再处理组（21.2 ± 0.3%，P < 0.05 与对照组相比）和 PMN 耗竭组（9.4 ± 0.3%，P < 0.05 与对照组相比）中减少，与对照组相比，再处理加 PMN 耗竭组（5.4 ± 0.6%，P < 0.05 与对照组相比）进一步减少。在犬中，PMN 在 R 时 2 小时和 24 小时的（•）O2 释放增加，后处理可将其降低至基线水平。
这些数据表明 PMN 参与了后处理的心脏保护作用。
