Reperfusion injury

1. Definition

• Reperfusion injury (再灟流障害) = paradoxical phenomenon where re-introducing O₂ (blood flow) to previously ischemic tissue accelerates necrosis instead of rescuing it.
• Clinically important because we routinely try to restore flow after ischemia.

2. Mechanism

1. Ischemic necrosis impairs antioxidant enzymes (catalase, superoxide dismutase, glutathione peroxidase).
2. When O₂ returns, these damaged enzymes cannot neutralise free radicals.
3. Reperfusion with incomplete O₂ reduction → burst of ROS (活性酸素種):
   • superoxide (O₂⁻), hydrogen peroxide (H₂O₂), hydroxyl radical (OH•)
4. ROS → lipid peroxidation, cross-linked proteins, DNA fragmentation → further cell damage.
5. Reperfused plasma proteins activate the complement system → cell lysis.
6. Ca²⁺ overload + mitochondrial injury amplify cell death.

3. Methods of Reperfusion

• Balloon angioplasty ± stent
• Thrombolysis (streptokinase, tPA)
• Arterial bypass

If performed in time, outcome is good. If late, reperfusion injury develops.

4. Consequences of Reperfusion Injury

• Provision of ROS (oxidative damage)
• Haemorrhage — post-ischemic vasculature is injured and leaky
• Capillary swelling → occlusion of flow (“no-reflow” phenomenon)
• Contraction band necrosis — hypercontracted sarcomeres because:
  • Ca²⁺ influx drives actin–myosin interaction
  • no ATP available to relax

💡 High-yield: Reperfusion injury matters most after thrombolysis/PCI in myocardial infarction and after recanalisation in stroke; contraction band necrosis is its classic myocardial hallmark.