Cerebral and myocardial mitochondrial injury differ in a rat model of cardiac arrest and cardiopulmonary resuscitation - 17/06/21
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Abstract |
Brain mitochondria are more sensitive to global ischemia compared to heart mitochondria. Complex I in the electron transport chain (ETC) is sensitive to ischemic injury and is a major control point of the rate of ADP stimulated oxygen consumption. The purpose of this study was to explore whether changes in cerebral and myocardial mitochondria differ after cardiac arrest. Animals were randomized into 4 groups (n = 6): 1) Sham 2) VF 3) VF+CPR 4) ROSC 1hr. Ventricular Fibrillation (VF) was induced through a guide wire advanced from the right jugular vein into the ventricle and untreated for 8 min. Resuscitation was attempted with a 4J defibrillation after 8 min of cardiopulmonary resuscitation (CPR). Brain mitochondria and cardiac mitochondrial subpopulations were isolated. Calcium retention capacity was measured to assess susceptibility to mitochondrial permeability transition pore opening. ADP stimulated oxygen consumption and ETC activity assays were performed. Brain mitochondria are far more sensitive to injury during cardiac arrest and resuscitation compared to cardiac mitochondria. Complex I is highly sensitive to injury in brain mitochondria. With markedly decreased calcium retention capacity, mitochondria contribute to cerebral reperfusion injury. Therapeutic preservation of cerebral mitochondrial activity and mitochondrial function during cardiac arrest may improve post-resuscitation neurologic function.
Le texte complet de cet article est disponible en PDF.Graphical Abstract |
Highlights |
• | Brain mitochondria are more sensitive to cardiac arrest than heart mitochondria. |
• | Complex I is highly sensitive to injury in brain mitochondria. |
• | Brain mitochondrial activity and functional preservation may improve outcomes. |
Keywords : Brain mitochondrial activity, Electron transport chain, Ischemia reperfusion injury, Mitochondrial permeability transition pore, ADP stimulated oxygen consumption
Plan
☆ | All work was performed at the Weil Institute of Emergency and Critical Care Research and at the laboratory of Dr. Edward Lesnefsky at Virginia Commonwealth University. |
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