Reperfusion injury following restoration of blood flow to ischemic myocardium is primarily mediated by:

• A Renewed ATP depletion and mitochondrial dysfunction alone
• B Reactive oxygen species (ROS) generated by xanthine oxidase and activated neutrophils causing further membrane and DNA damage ✓
• C Complement C5b-9 membrane attack complex in the absence of free radicals
• D Calcium influx alone without free radical generation

Explanation

Reperfusion injury is paradoxical worsening of ischemic damage upon reoxygenation. The key mediators are reactive oxygen species: xanthine oxidase (converted from xanthine dehydrogenase during ischemia) generates superoxide upon reoxygenation, and recruited neutrophils release additional ROS and proteases. Calcium overload and opening of the mitochondrial permeability transition pore also contribute, but ROS generation is the primary and most targetable mechanism.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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