Weil Brian R, Young Rebeccah F, Shen Xiaomeng, Suzuki Gen, Qu Jun, Malhotra Saurabh, Canty John M
Department of Physiology & Biophysics, University at Buffalo, Buffalo, NY USA.
The Clinical and Translational Research Center of the University at Buffalo, Buffalo, NY USA.
JACC Basic Transl Sci. 2017 Apr;2(2):105-114. doi: 10.1016/j.jacbts.2017.01.006. Epub 2017 Mar 29.
In a porcine model of brief ischemia leading to reversible stunning in the absence of tissue necrosis, we demonstrated delayed release of cTnI that exceeded the 99 percentile for normals 60-minutes after reperfusion and rose to readily detectable levels 24-hours later. While tissue analysis at 60-minutes showed no evidence of infarction, TUNEL staining demonstrated isolated myocytes undergoing apoptosis, which was absent after 24-hours. These results demonstrate that cTnI elevations occur after ischemia of a duration that is insufficient to produce myocyte necrosis and reflect myocyte injury associated with delayed apoptosis in the absence of pathological evidence of infarction.
在一个猪模型中,短暂缺血导致可逆性心肌顿抑且无组织坏死,我们证明了肌钙蛋白I(cTnI)延迟释放,在再灌注60分钟后超过正常水平的第99百分位数,并在24小时后升至易于检测的水平。虽然60分钟时的组织分析未显示梗死迹象,但TUNEL染色显示有孤立的心肌细胞发生凋亡,24小时后则不存在这种情况。这些结果表明,在缺血持续时间不足以产生心肌细胞坏死的情况下,cTnI会升高,这反映了在没有梗死病理证据的情况下与延迟凋亡相关的心肌细胞损伤。