Department of Physiology and Cell Biology, Ohio State University, Columbus, Ohio 43210-1218, USA.
J Appl Physiol (1985). 2012 Sep 1;113(5):766-74. doi: 10.1152/japplphysiol.01424.2011. Epub 2012 Jul 5.
Hydroxyl radicals (OH) are involved in the pathogenesis of reperfusion injury and are observed in acute heart failure, stroke, and myocardial infarction. Two different subcellular defects are involved in the pathogenesis of OH injury, deranged calcium handling, and alterations of myofilament responsiveness, but their temporal impact on contractile function is not resolved. Initially, after brief OH exposure, there is a corresponding marked increase in diastolic calcium and diastolic force. We followed these parameters until a new steady-state level was reached at ~45 min post-OH exposure. At this new baseline, diastolic calcium had returned to near-normal, pre-OH levels, whereas diastolic force remained markedly elevated. An increased calcium sensitivity was observed at the new baseline after OH-induced injury compared with the pre-OH state. The acute injury that occurs after OH exposure is mainly due to calcium overload, while the later sustained myocardial dysfunction is mainly due to the altered/increased myofilament responsiveness.
羟基自由基（OH）参与再灌注损伤的发病机制，在急性心力衰竭、中风和心肌梗死中都有观察到。OH 损伤的发病机制涉及两种不同的亚细胞缺陷，即钙处理紊乱和肌丝反应性改变，但它们对收缩功能的时间影响尚未得到解决。最初，在短暂的 OH 暴露后，舒张钙和舒张力会相应地显著增加。我们一直跟踪这些参数，直到 OH 暴露后约 45 分钟达到新的稳定状态水平。在这个新的基线水平上，舒张钙已经恢复到 OH 前的接近正常水平，而舒张力仍然明显升高。与 OH 前状态相比，OH 诱导损伤后的新基线水平观察到钙敏感性增加。OH 暴露后发生的急性损伤主要是由于钙超载，而后期持续的心肌功能障碍主要是由于肌丝反应性改变/增加。
