科研之友
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摘要
Background: Postconditioning (postcon) reduces infarct size, myocardial superoxide ((center dot)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 (center dot)O(2) generation. %26lt;br%26gt;Methods: 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 (center dot)O(2) by luminol-enhanced chemiluminescence. %26lt;br%26gt;Results: Postcon and PMN depletion reduced infarct size (42.6 +/- 2.1%, P %26lt; 0.05 vs. control, and 43.9 +/- 3.0%, P %26lt; 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 %26lt; 0.05 vs. control) and PMN-depleted (9.4 +/- 0.3%, P %26lt; 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 %26lt; 0.05 vs. control). In dogs, (center dot)O(2) release by PMNs increased at 2 h and 24 h of R, which was reduced to baseline levels by postcon. %26lt;br%26gt;Conclusions: These data imply PMN involvement in cardioprotection by postconditioning.
- 出版日期2012-1
