Reperfusion injury after myocardial ischemia is primarily mediated by:

• A Continued ATP depletion preventing membrane pump recovery after flow is restored
• B Burst of reactive oxygen species from dysfunctional mitochondria and xanthine oxidase upon reoxygenation ✓
• C Lactic acidosis leading to lysosomal enzyme release and autodigestion
• D Complement-independent neutrophil margination causing microvascular plugging

Explanation

Reperfusion injury paradoxically worsens damage upon restoration of blood flow. Sudden reintroduction of oxygen to ischemic cells generates a burst of ROS from dysfunctional mitochondria and activated xanthine oxidase. ROS cause membrane lipid peroxidation, protein oxidation, and DNA damage. Opening of the mitochondrial permeability transition pore (mPTP) upon reperfusion is an additional key mechanism triggering cardiomyocyte death.

Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.