Cardiac arrest (CA) induces whole-body ischemia resulting in mitochondrial dysfunction. We used isolated mitochondria to examine phospholipid alterations in the brain, heart, kidney, and liver post-CA. Our data shows that ischemia/reperfusion most significantly alters brain mitochondria phospholipids, predominately after resuscitation. Furthermore, the alterations do not appear to be a function of dysregulated importation of phospholipids, but caused by impaired intra-mitochondrial synthesis and/or remodeling of phospholipids. Our data demonstrates only brain mitochondria undergo significant alterations in phospholipids, providing a rationale for the high vulnerability of the brain to ischemia/reperfusion. Furthermore, analyzing this pathophysiologic state provides insight into physiologic mitochondrial phospholipid metabolism.

心脏骤停 (CA) 诱导全身缺血，导致线粒体功能障碍。我们使用分离的线粒体来检查 CA 后大脑、心脏、肾脏和肝脏中的磷脂变化。我们的数据显示，缺血/再灌注对脑线粒体磷脂的改变最为显着，主要是在复苏后。此外，这些改变似乎不是磷脂输入失调的功能，而是由线粒体内合成受损和/或磷脂重塑引起的。我们的数据表明，只有脑线粒体的磷脂发生显着变化，这为大脑对缺血/再灌注的高度脆弱性提供了依据。此外，分析这种病理生理状态可以深入了解生理性线粒体磷脂代谢。