Ischemic preconditioning depends on age and gender.

Ischemic preconditioning depends on age and gender.
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缺血预处理取决于年龄和性别。

DOI:
10.1007/s00395-006-0585-4
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发表时间:
2006
影响因子:
9.5
通讯作者:
Baker,AJ
Baker,AJ
中科院分区:
医学1区
文献类型:
--
作者:
Turcato,S;Turnbull,L;Wang,G-Y;Honbo,N;Simpson,PC;Karliner,JS;Baker,AJ

文献摘要

相似文献

这项研究的目的是确定缺血预适应(IPC)方案是否能改善雌性小鼠心脏缺血后的功能恢复。之前的一项研究发现,10周大的雌性婴儿的心脏不会发生IPC。我们研究了10周龄和18周龄小鼠(雄性和雌性)的兰登多夫灌流心脏。心肌缺血45min再灌流(I/R),缺血预适应3min。我们测量了血流动力学、梗死灶大小和磷酸化存活蛋白Akt(p-Akt)的水平。与之前的研究类似,对于10周大的小鼠,我们发现IPC方案显著改善了雄性而不是雌性小鼠心脏的左心室发展压(LVdP)的恢复。然而,对于18周大的小鼠,我们发现IPC方案使雄性和雌性的LVDP恢复都翻了一番。在这两个年龄段,与男性相比,女性心脏的LVDP恢复更快,p-Akt水平更高。结论这些发现与越来越多的证据一致,即缺血或其他干预措施诱导的预适应可以发生在女性心脏中。然而,对于女性的心脏来说,预适应取决于年龄。此外,与之前的研究一致,女性心脏对缺血损伤具有更强的内在抵抗力,可能涉及通过p-Akt增加信号。
The goal of this study was to determine if an ischemic preconditioning (IPC) protocol improved post–ischemic functional recovery of female mouse hearts. A previous study found that IPC did not occur in hearts from 10–week–old females. We studied Langendorff–perfused hearts from both 10– and 18–week–old mice (males and females). Hearts were subjected to 45 min ischemia and 45 reperfusion (I/R); IPC involved pretreatment with 3 min ischemia. We measured hemodynamics, infarct size and levels of the phosphorylated prosurvival kinase Akt (p–Akt). Similar to a previous study, for 10– week–old mice we found that the IPC protocol appreciably improved recovery of LV developed pressure (LVDP) for hearts from males but not females. However, for 18–week–old mice we found that the IPC protocol doubled the recovery of LVDP for both males and females. For both ages, hearts from females had greater recovery of LVDP and higher levels of p–Akt compared to males.ConclusionsThese findings are consistent with growing evidence that preconditioning induced by ischemia or other interventions can occur in hearts from females. However, for hearts from females, preconditioning depends on age. Moreover, consistent with previous studies, hearts from females have greater inherent resistance to ischemic injury, possibly involving increased signaling via p–Akt.