During reperfusion injury after myocardial ischemia, which mechanism is primarily responsible for cardiomyocyte death that was not irreversibly injured during the ischemic phase itself?
- A ATP depletion causing failure of Na-K ATPase
- B Coagulative necrosis from direct acid accumulation
- C Mitotic catastrophe from DNA strand breaks
- D Calcium overload mediated by mitochondrial permeability transition pore (mPTP) opening ✓
Explanation
Reperfusion injury involves paradoxical cell death upon restoration of blood flow, driven largely by massive calcium influx and ROS generation. Calcium overload activates the mitochondrial permeability transition pore (mPTP), causing inner membrane permeabilization, dissipation of the proton gradient, mitochondrial swelling, and release of cytochrome c triggering apoptosis. ROS also cause lipid peroxidation and protein damage. This is distinct from the purely ischemic mechanism of ATP depletion and Na-K ATPase failure.
Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.