文摘

老化的心是已知减少能力防止再氧化缺血/再灌注(IR)损伤提供了各种心血管治疗方案。寻找一个更成功的方案,我们研究了年龄的反应心预处理(PC)和后处理(POST)引起鞘氨醇或鞘氨醇1-phosphate治疗。体外大鼠心脏模型被用来研究电脑的能力和保护老的心(每月27日)后对I / R损伤由40分钟(min)指数缺血再灌注的40分钟紧随其后。缺血性电脑的反应是减少在27个月心相对于3 - 6月(年轻)的心所指出的一个贫穷的复苏开发的左心室压力(LVDP)对再灌注在年轻的心(45%比74%)和一个大梗塞大小40分钟后再灌注在年轻的心(37%比8%)。PC与鞘氨醇1-phosphate (S1P)也可怜的老心LVDP和27%的收益率只有49%复苏梗塞大小。相比之下,个人电脑与鞘氨醇受老化影响;78%恢复LVDP和8%梗塞大小没有不同于年轻的心。缺血后比缺血性PC被老化的影响较小,但老的心仍然经历了梗塞大小的28%。的老心S1P也伴随着大量梗塞大小(24%)。然而,旧的心与鞘氨醇优于其他形式的文章,因为它减少了梗塞大小为12%。 S1P levels were found to be lower in old hearts which may contribute to the decreased effectiveness of ischemic PC and POST. Further, phospho-Akt levels and distribution were altered in response to cardioprotection in the old hearts. In conclusion, POST was less affected by aging than PC; and sphingosine is a uniquely effective agent for both PC and POST of aging hearts.