Reperfusion injury after myocardial infarction causes additional cell death largely through which primary mechanism?
- A Resumption of ATP synthesis causing explosive osmotic lysis
- B Burst of reactive oxygen species from re-energized mitochondria and xanthine oxidase ✓
- C Abrupt restoration of neutral pH killing acidosis-adapted cells
- D Complement activation by antibodies against neoantigens
Correct answer: B. Burst of reactive oxygen species from re-energized mitochondria and xanthine oxidase
Explanation
On reperfusion, re-energized mitochondria generate a burst of reactive oxygen species (ROS) that damage membranes, proteins, and DNA in already-injured cells. Xanthine oxidase, activated during ischemia, also generates ROS on oxygen reintroduction. Additionally, calcium overload and mitochondrial permeability transition pore (mPTP) opening contribute. Paradoxically, restoration of pH is now recognized to accelerate mPTP opening, compounding injury.
Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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